Medicurio

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INTRODUCTION-

Urinary incontinence happens when you lose control of your bladder. In some cases, you may empty your bladder’s contents completely. In other cases, you may experience only minor leakage. The condition may be temporary or chronic, depending on its cause.

According to the Urology Care Foundation, millions of adults in the United States experience urinary incontinence. According to Johns Hopkins Medicine, it’s more common among women age 50 and over. However, this condition can affect anyone.

As you age, the muscles supporting your bladder tend to weaken, which can lead to urinary incontinence.

Many different health problems can also cause the condition. Symptoms can range from mild to severe and can be a sign of cancer, kidney stones, infection, or an enlarged prostate.

If you experience urinary incontinence, make an appointment with your healthcare provider. Urinary incontinence can interfere with your daily life and lead to potential accidents. Your healthcare provider can also determine if a more serious medical condition is the cause.

Urinary incontinence — the loss of bladder control — is a common and often embarrassing problem. The severity ranges from occasionally leaking urine when you cough or sneeze to having an urge to urinate that’s so sudden and strong you don’t get to a toilet in time.

Though it occurs more often as people get older, urinary incontinence isn’t an inevitable consequence of aging. If urinary incontinence affects your daily activities, don’t hesitate to see your doctor. For most people, simple lifestyle changes or medical treatment can ease discomfort or stop urinary incontinence.

TYPES-

Urinary incontinence is divided into three general types. You can potentially experience more than one type at the same time.

Stress incontinence

Stress incontinence is triggered by certain types of physical activity.

For example, you might lose control of your bladder when you’re:

• exercising
• coughing
• sneezing
• laughing

Such activities put stress on the sphincter muscle that holds urine in your bladder. The added stress can cause the muscle to release urine.

Urge incontinence

Urge incontinence occurs when you lose control of your bladder after experiencing a sudden and strong urge to urinate. Once that urge hits, you may not be able to make it to the bathroom in.

Overflow incontinence

Overflow incontinence can occur if you don’t completely empty your bladder when you urinate. Later, some of the remaining urine may leak from your bladder. This type of incontinence is sometimes called “dribbling.”

Mixed Incontinence

Some people have more than one type of urinary incontinence. Some people leak urine both with strong physical activity (SUI) AND have a strong uncontrollable sense of urgency (OAB.) This is mixed urinary incontinence. This person has both SUI and OAB. In this case, it helps to know what is occurring and what is causing leaks to learn how to manage problems.

CAUSES-

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Urinary incontinence isn’t a disease, it’s a symptom. It can be caused by everyday habits, underlying medical conditions or physical problems. A thorough evaluation by your doctor can help determine what’s behind your incontinence.

Temporary urinary incontinence

Certain drinks, foods and medications may act as diuretics — stimulating your bladder and increasing your volume of urine. They include:

• Alcohol
• Caffeine
• Carbonated drinks and sparkling water
• Artificial sweeteners
• Chocolate
• Chili peppers
• Foods that are high in spice, sugar or acid, especially citrus fruits
• Heart and blood pressure medications, sedatives, and muscle relaxants
• Large doses of vitamin C

Urinary incontinence may also be caused by an easily treatable medical condition, such as:

• Urinary tract infection. Infections can irritate your bladder, causing you to have strong urges to urinate, and sometimes incontinence.
• Constipation. The rectum is located near the bladder and shares many of the same nerves. Hard, compacted stool in your rectum causes these nerves to be overactive and increase urinary frequency.

Persistent urinary incontinence

Urinary incontinence can also be a persistent condition caused by underlying physical problems or changes, including:

• Pregnancy. Hormonal changes and the increased weight of the fetus can lead to stress incontinence.
• Childbirth. Vaginal delivery can weaken muscles needed for bladder control and also damage bladder nerves and supportive tissue, leading to a dropped (prolapsed) pelvic floor. With prolapse, the bladder, uterus, rectum or small intestine can get pushed down from the usual position and protrude into the vagina. Such protrusions can be associated with incontinence.
• Changes with age. Aging of the bladder muscle can decrease the bladder’s capacity to store urine. Also, involuntary bladder contractions become more frequent as you get older.
• Menopause. After menopause women produce less estrogen, a hormone that helps keep the lining of the bladder and urethra healthy. Deterioration of these tissues can aggravate incontinence.
• Hysterectomy. In women, the bladder and uterus are supported by many of the same muscles and ligaments. Any surgery that involves a woman’s reproductive system, including removal of the uterus, may damage the supporting pelvic floor muscles, which can lead to incontinence.
• Enlarged prostate. Especially in older men, incontinence often stems from enlargement of the prostate gland, a condition known as benign prostatic hyperplasia.
• Prostate cancer. In men, stress incontinence or urge incontinence can be associated with untreated prostate cancer. But more often, incontinence is a side effect of treatments for prostate cancer.
• Obstruction. A tumor anywhere along your urinary tract can block the normal flow of urine, leading to overflow incontinence. Urinary stones — hard, stone-like masses that form in the bladder — sometimes cause urine leakage.
• Neurological disorders. Multiple sclerosis, Parkinson’s disease, a stroke, a brain tumor or a spinal injury can interfere with nerve signals involved in bladder control, causing urinary incontinence.

There are many potential causes of urinary incontinence.

Examples include:

• weakened bladder muscles, resulting from aging
• physical damage to your pelvic floor muscles
• enlarged prostate
• cancer

Some of these conditions are easily treatable and only cause temporary urinary problems. Others are more serious and persistent.

Aging

As you get older, the muscles supporting your bladder typically become weaker, which raises your risk for incontinence.

To maintain strong muscles and a healthy bladder, it’s important to practice healthy lifestyle habits. The healthier you are, the better your chances of avoiding incontinence as you age.

Damage

Your pelvic floor muscles support your bladder. Damage to these muscles can cause incontinence. It can be caused by certain types of surgery, such as a hysterectomy. It’s also a common result of pregnancy and childbirth.

Enlarged prostate

If you’re male, your prostate gland surrounds the neck of your bladder. This gland releases fluid that protects and nourishes your sperm. It tends to enlarge with age. It’s common for males to experience some incontinence as a result.

Cancer

Prostate or bladder cancer can cause incontinence. In some cases, treatments for cancer can also make it harder for you to control your bladder. Even benign tumors can cause incontinence by blocking your flow of urine.

Other potential causes

Other potential causes of incontinence include:

• constipation
• urinary tract infections (UTIs)
• kidney or bladder stones
• prostatitis, or inflammation of your prostate
• interstitial cystitis, or a chronic condition that causes inflammation within your bladder
• side effects from certain medications, such as blood pressure drugs, muscle relaxants, sedatives, and some heart medications

Some lifestyle factors can also cause temporary bouts of incontinence. For example, drinking too much alcohol, caffeinated beverages, or other fluids can cause you to temporarily lose control of your bladder.

DIAGNOSIS-

A urologist or primary care doctor will start by asking questions. They will want to know about your symptoms and your medical history. They will ask about your health habits and fluid intake. They will also want to know how much your incontinence has changed your quality of life.

A good medical history, physical exam and a few simple tests are most often all that is needed to diagnose the cause of incontinence. A complete review of the medications you are taking may reveal one that alters normal bladder or urethral function. Your doctor may test your urine for bacteria or blood (urinalysis) to look for a urinary tract infection or other source of irritation to the bladder.

A cough stress test may be performed to check for SUI. A simple bladder ultrasound test to see how well you empty your bladder is often performed. Or a more involved “stress test” for the bladder can be done in more complicated cases (urodynamic test) to better see just how your bladder and urethra work. Other conditions to look for include vaginal hernias or pelvic organ prolapse (POP), and major bowel problems, such as constipation or fecal incontinence.

A urologist or primary care doctor will start by asking questions. They will want to know about your symptoms and your medical history. They will ask about your health habits and fluid intake. They will also want to know how much your incontinence has changed your quality of life.

A good medical history, physical exam and a few simple tests are most often all that is needed to diagnose the cause of incontinence. A complete review of the medications you are taking may reveal one that alters normal bladder or urethral function. Your doctor may test your urine for bacteria or blood (urinalysis) to look for a urinary tract infection or other source of irritation to the bladder.

A cough stress test may be performed to check for SUI. A simple bladder ultrasound test to see how well you empty your bladder is often performed. Or a more involved “stress test” for the bladder can be done in more complicated cases (urodynamic test) to better see just how your bladder and urethra work. Other conditions to look for include vaginal hernias or pelvic organ prolapse (POP), and major bowel problems, such as constipation or fecal incontinence.

A cough stress test may be performed to check for SUI. A simple bladder ultrasound test to see how well you empty your bladder is often performed. Or a more involved “stress test” for the bladder can be done in more complicated cases (urodynamic test) to better see just how your bladder and urethra work. Other conditions to look for include vaginal hernias or pelvic organ prolapse (POP), and major bowel problems, such as constipation or fecal incontinence.

Risk factors

Factors that increase your risk of developing urinary incontinence include:

• Gender. Women are more likely to have stress incontinence. Pregnancy, childbirth, menopause and normal female anatomy account for this difference. However, men with prostate gland problems are at increased risk of urge and overflow incontinence.
• Age. As you get older, the muscles in your bladder and urethra lose some of their strength. Changes with age reduce how much your bladder can hold and increase the chances of involuntary urine release.
• Being overweight. Extra weight increases pressure on your bladder and surrounding muscles, which weakens them and allows urine to leak out when you cough or sneeze.
• Smoking. Tobacco use may increase your risk of urinary incontinence.
• Family history. If a close family member has urinary incontinence, especially urge incontinence, your risk of developing the condition is higher.
• Other diseases. Neurological disease or diabetes may increase your risk of incontinence.

Complications

Complications of chronic urinary incontinence include:

• Skin problems. Rashes, skin infections and sores can develop from constantly wet skin.
• Urinary tract infections. Incontinence increases your risk of repeated urinary tract infections.
• Impacts on your personal life. Urinary incontinence can affect your social, work and personal relationships.

Prevention

Urinary incontinence isn’t always preventable. However, to help decrease your risk:

• Maintain a healthy weight
• Practice pelvic floor exercises
• Avoid bladder irritants, such as caffeine, alcohol and acidic foods
• Eat more fiber, which can prevent constipation, a cause of urinary incontinence
• Don’t smoke, or seek help to quit smoking

TREATMENT-

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There are many ways to help you take control over your bladder. You may not need to wear pads or diapers. Some problems are short-term and can be easily relieved. Others take more time to treat. Treatments range from lifestyle changes to bladder training to medications to simple procedural therapies to surgery.

Lifestyle Changes

Lifestyle changes, such as changing your diet, should be tried first. With lifestyle changes, you change the way you live day-to-day. This may include what you eat or drink, or practicing other methods that may control symptoms. You may not get rid of all symptoms with lifestyle changes, but your symptoms may feel better after changing a few habits. For some, weight loss has been linked to helping urinary symptoms.

Fluid Control

You will likely be asked to track what you drink, when and how much. You may learn that you should limit certain things such as caffeine and alcohol. These drinks may bother the bladder. You may also be asked to drink more water. Six to eight glasses of water per day is ideal. Also, you may be asked not to drink for a few hours before bed. This will help reduce your need to get up and go to the bathroom at night.

Limit Certain Foods and Drinks

Some foods and drinks have been found, anecdotally, as irritants to the bladder. Some people have found spicy foods, coffee, tea and colas to be bothersome. However, studies have not proven that these are really “bladder irritants” in all patients. A good plan is for you to try to notice on your own how different food and drinks effect you and your symptoms.

Bladder Training

A bladder diary is the starting point for bladder training. For 3 days, you write down what and how much you drink, and how often you go to the bathroom. Noting when you leak urine can also be helpful. This diary can help you and your provider find things that may make your symptoms worse. It can also help your provider build a bladder training plan for you. This is when you empty your bladder in a controlled way at set times. When you empty your bladder as a routine, you should have less leaks. Timed urination, scheduled voiding or double voiding are methods that can help with both OAB and SUI.

If you go to the bathroom too often, retraining your bladder can help. The goal is to hold your urine in the bladder for longer and longer amounts of time. This takes small steps. Start with adding 5 to 10 minutes. The goal is to retrain your bladder to hold urine for 3 to 4 hours, with less urgency and leaking.

Pelvic Floor Exercises

Kegel exercises can strengthen the urethral sphincter and pelvic floor muscles. This works for both men and women. If you can learn to tighten and relax these muscles, this can often help your bladder control.

Kegels can also help control the bladder spasms that trigger the urge to go. Squeezing the pelvic floor muscles inspires a reflex to the bladder to get the bladder to quiet down, to help suppress the urge feeling. This can pause or even stop the uncontrollable UUI leaks. A health care provider can teach you how to do these exercises with success.

Kegels can help with both SUI (by making the muscles strong) and OAB/UUI (by suppressing the urge feeling). Like any fitness program, you must practice the exercises often to keep helping your body.

Medical Treatments

When lifestyle changes do not help enough, your health care provider may ask you to try prescription medications. A frank talk with your provider about the risks, side effects and benefits of each medication will help you decide which might be the right one for you.

Anticholinergic Drugs

Anticholinergic drugs treat OAB/UUI by helping the bladder muscle to relax. Common medications include oxybutynin, tolterodine and solifenacin. They work well for the bladder, but are also linked to many bothersome side effects such as dry mouth, constipation, blurred vision, and lately, some concern for causing confusion or dementia with longer-term use. Trospium chloride does not diffuse into the brain so is not thought to have a risk of confusion or dementia.

A newer medication for OAB is merbegron. It is not an anticholinergic medication, so it is not linked to any of the side effects described above. It is an alpha-agonist, so works a little differently on the bladder, but in the end has the same effect of getting the bladder to relax. It can cause increases in blood pressure so needs to be used with caution in patients with hypertension.

Be sure to talk about any bladder relaxing drugs you have tried when you talk with your urologist.

Hormone Treatment

For women, local vaginal/urethral estrogen therapy can help if you are having urinary incontinence after menopause. Estrogen replacement helps the health of the walls of the vagina, the bladder neck and the urethra. This may ease irritative bladder symptoms and incontinence. There are some special medical reasons not to use local hormones, so be sure to speak to your provider about what is best for you.

Surgical Treatments for SUI

Choosing to have surgery is very personal. If surgery is suggested, there are many choices. It helps to learn as much as you can before you decide. You should work with a doctor who has experience in SUI surgery. Learn the risks and benefits of all your surgical choices, as well as what to expect during and after surgery, to make the most informed choice that will be best for you.

Slings

• Female Sling

The most common surgical treatment and the current standard of care for the surgical treatment of female SUI is the midurethral sling surgery. For this, a strip of soft permanent mesh is placed under the urethra to support urethral closure during actions that involve “physical pelvic stress” (coughing, sneezing, bending, lifting, jumping and running). It is a simple 10-20 minute, outpatient procedure with a small single-cut in the vagina. This is easily done under limited anesthesia and linked to a very quick return to normal day-to-day activities. Long-term success rates are in the 90%.

Another type of female sling surgery, the pubovaginal sling, is a bladder neck sling. Here the tissue used to make the sling comes from the patient’s abdominal wall (fascia), or donated tissue (bovine or cadaver).

• Male Sling

A sling procedure may be offered to treat SUI in some men. The male sling is for urethral sphincter muscle support. For this, a soft mesh tape is placed under the urethra through a cut between the scrotum and rectum. It supports the urethra and sphincter muscle by pushing up on the urethra and causing some coaptation (closure) of the urethra to prevent leaks. Ask your healthcare provider if this is an option for you.

Bladder Neck Suspension / Colposuspension

The Burch Colposuspension, or bladder neck suspension, is surgery for female SUI that lifts the bladder neck up towards the pubic bone with permanent stitches. This is a bigger surgery with a cut through the abdominal wall (muscles and skin), to reach the deeper pelvic areas. Because of the cut into the belly, it takes a longer time to heal from this surgery compared to the more minimally invasive midurethral sling, but it can be the right choice for some patients. In some cases it can be performed laparoscopically, which lessens the recovery time after surgery.

Bulking Agents (Injections)

This option is used to treat female SUI by “bulking up” the inner urethral lining and making the opening of the urethra smaller. Modern bulking agents are permanent materials that are placed into the tissues around the urethra and sphincter muscle up towards the bladder neck. This helps how well the natural urethral closure function can work to stop leaks.

Note that bulking agents are not FDA-approved for male SUI.

Artificial Urinary Sphincter

The most common treatment for male SUI is to implant a device around the urethra called an artificial urinary sphincter (AUS). In some cases, women may also be helped from this surgery, but due to other surgical options mentioned earlier, this is rarely needed in women. The AUS is a device with three parts:

1. An artificial urinary sphincter, which is a fluid filled cuff placed around the urethra.
2. A fluid-filled, pressure-sensing balloon that joins to the cuff and regulates the pressure within the cuff. This balloon is placed in the lower abdomen.
3. A pump placed in the scrotum for men (and labia for women), that transfers the fluid between the cuff and the balloon to open and close the cuff (artificial urinary sphincter). The pump is easily controlled by the patient.

At rest, the AUS cuff is closed (full of fluid) to prevent leaks. When you decide to empty your bladder, you activate the pump to push fluid from the cuff to the balloon that holds your urine. This allows the urethra to open so that the urine can flow through and empty the bladder. This surgery can cure or greatly help urinary control in about 70-80% of men. If you have had radiation, scar tissue in the urethra, or other bladder problems then this option may not be the best option for you.

Surgical Treatments for OAB

If lifestyle changes and medicine are not working for your OAB, there are other options. A trained urologist or female pelvic medicine & reconstructive surgery (FPMRS) specialist can help.

Bladder Botox® Treatment

Your doctor may offer bladder Botox® (onabotulinumtoxin). Botox works for the bladder to relax the muscle of the bladder wall to reduce urinary urgency and urge incontinence. To put Botox into the bladder your doctor will use a small camera, a cystoscope, through the urethra and into the bladder. With a tiny needle attached to the cystoscope, the Botox is injected in small amounts straight into the wall of the bladder, spreading it out evenly throughout the bladder. This procedure is most often performed in the office with local anesthesia (numbing mixture in the bladder). The effects of Botox last about 6-9 months, so repeat treatments will be needed when OAB symptoms return.

Within a few weeks of the treatment, your health care provider will want to check to see how well it is working for you, and to make sure you are still able to empty your bladder well. A small amount (<10%) of patients have trouble emptying their bladder for a short time after the treatment and may need to use a catheter (small tube) until their voiding improves.

Nerve Stimulation

Another treatment for people who need extra help for their OAB is nerve stimulation, also called neuromodulation therapy. This type of treatment sends electrical pulses to nerves that share the same path for the bladder (pelvic nerves). In OAB, the nerve signals between your bladder and brain do not always communicate the right way. Treatment with electrical pulses help to modulate the neurological signaling so the brain and the pelvic nerves can communicate better to help the bladder function – to “calm down” — and help OAB symptoms.

There are two main types available today:

• Percutaneous Tibial Nerve Stimulation (PTNS)

Percutaneous Tibial Nerve Stimulation, or PTNS, (peripheral) is an easy way to modulate the nerves to your bladder. PTNS is performed in the office, with each session taking about 30 minutes. PTNS is done by placing a small needle electrode in your lower leg near your ankle. It sends stimulation pulses up the leg, by way of the tibial nerve, to the pelvic nerves that modulate the bladder function to “calm the bladder down.” The therapy is approved as a program of weekly 30 minute sessions for 12 treatments, followed by on-going monthly care treatment sessions to keep the benefits.

• Sacral Nerve Stimulation (SNS)

SNS (central) stimulates the pelvic nerves by way of direct sacral nerve stimulation – the nerve root coming right off the spinal cord. Stimulation here again serves to modulate the neurological signaling between the bladder and the brain to help bladder function. SNS involves an implantable bladder pacemaker to control these signals to stop OAB symptoms. SNS is a two-step surgical process, which gives patients the chance to try the therapy first before making choices about final surgical implantation of the pacemaker. The first step is to implant an electrical wire through the skin in your lower back that goes deep towards the sacral nerves. This wire is linked to an external, handheld pacemaker for the test. If it helps sufficiently for your OAB symptoms, the second step is to join the wire to an implantable permanent pacemaker. The stimulation is then continuous as it regulates the pelvic nerve activity to control the OAB symptoms.

Bladder Reconstruction / Urinary Diversion Surgery

These type of major abdominal surgeries are only used in very rare and complicated cases. There are two main categories of major abdominal surgery. The goal of augmentation cystoplasty is to make the bladder bigger to increase how much urine it can hold at any one time. The goal of urinary diversion is to re-route the flow of urine away from the bladder and often results in a stoma and external appliance to catch the urine. There are many risks to these surgeries, so it is offered only when no other option can help.

Surgical Treatments for Overflow Incontinence

Overflow urinary incontinence happens when the bladder cannot empty well and dribbles as the bladder pressure grows. Most often, it is linked to some type of block of the bladder neck and/or urethra, and requires some type of procedural or surgical action to fix the block. Common problems in men that can lead to holding urine in and overflow incontinence include an enlarged prostate (benign prostatic hyperplasia, BPH) and urethral strictures. It is quite rare for urethral strictures to happen in women. Other medical problems can change how the bladder contracts to empty, which can also lead to overflow incontinence.

You should speak with your urologist to learn what therapy might be right for you.

Products and Devices

For some people, incontinence products and devices are the only way to manage bladder problems to give you more freedom to do the things you want to do.

Some include:

• Indwelling catheter (stays in your body day and night, joined to a drainage bag)
• Intermittent catheters that are used many times each day
• External collecting systems (condom style for men, funnel and pouch for women)
• Absorbent products (pads, adult diapers, tampons)
• Pessaries for women, mostly those designed for SUI
• Toilet substitutes (like portable commodes)

Whatever your urinary problem is, there are likely good choices for you. It is vital to find a provider that specializes in bladder and incontinence problems, such as a urologist.

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Pelvic floor dysfunction is the inability to correctly relax and coordinate your pelvic floor muscles to have a bowel movement. Symptoms include constipation, straining to defecate, having urine or stool leakage and experiencing a frequent need to pee. Initial treatments include biofeedback, pelvic floor physical therapy and medications.

INTRODUCTION-

Pelvic floor dysfunction is a common condition where you’re unable to correctly relax and coordinate the muscles in your pelvic floor to urinate or to have a bowel movement. If you’re a woman, you may also feel pain during sex, and if you’re a man you may have problems having or keeping an erection (erectile dysfunction or ED). Your pelvic floor is a group of muscles found in the floor (the base) of your pelvis (the bottom of your torso).

If you think of the pelvis as being the home to organs like the bladder, uterus (or prostate in men) and rectum, the pelvic floor muscles are the home’s foundation. These muscles act as the support structure keeping everything in place within your body. Your pelvic floor muscles add support to several of your organs by wrapping around your pelvic bone. Some of these muscles add more stability by forming a sling around the rectum.

The pelvic organs include:

• The bladder (the pouch holding your urine).
• The uterus and vagina (in women).
• The prostate (in men).
• The rectum (the area at the end of the large intestine where your body stores solid waste).

Normally, you’re able to go to the bathroom with no problem because your body tightens and relaxes its pelvic floor muscles. This is just like any other muscular action, like tightening your biceps when you lift a heavy box or clenching your fist.

But if you have pelvic floor dysfunction, your body keeps tightening these muscles instead of relaxing them like it should. This tension means you may have:

• Trouble evacuating (releasing) a bowel movement.
• An incomplete bowel movement.
• Urine or stool that leaks.

As many as 50 percent of people with chronic constipation have pelvic floor dysfunction (PFD) — impaired relaxation and coordination of pelvic floor and abdominal muscles during evacuation. Straining, hard or thin stools, and a feeling of incomplete elimination are common signs and symptoms. But because slow transit constipation and functional constipation can overlap with PFD, some patients may also present with other signs and symptoms, such as a long time between bowel movements and abdominal pain.

When mechanical, anatomic, and disease- and diet-related causes of constipation have been ruled out, clinical suspicion should be raised to the possibility that PFD is causing or contributing to constipation. A focused history and digital examination are key components in diagnosing PFD. The diagnosis can be confirmed by anorectal manometry with balloon expulsion and, in some cases, traditional proctography or dynamic magnetic resonance imaging defecography to visualize pathologic pelvic floor motion, sphincter anatomy and greater detail of surrounding structures.

To help patients restore normal bowel function, Mayo Clinic staff use a multidisciplinary approach that can include:

• Constipation education classes led by a dietitian and a nurse educator
• Intensive pelvic floor retraining exercises
• Biofeedback training
• Behavior modification

Patients may meet individually with a dedicated nurse educator who provides a focused session on bowel management techniques. Central to the process is a daily regimen that combines an evening dose of fiber supplement with a morning routine of mild physical activity; a hot, preferably caffeinated beverage; and, possibly, a fiber cereal followed by another cup of a hot beverage — all within 45 minutes of waking. This routine augments early morning high-amplitude peristaltic contractions by incorporating multiple colon stimulators.

The regimen, useful for many types of constipation, is fine-tuned for PFD. Some patients do not need fiber; others may need to supplement with occasional laxatives. The program can change over time as patients make advancements.

Biofeedback to retrain pelvic floor muscles

Once patients with pelvic floor constipation have these basic tools, they can begin retraining the pelvic floor muscles with biofeedback. Based on the principle of operant conditioning, biofeedback provides auditory and visual feedback to help retrain the pelvic floor and relax the anal sphincter. Biofeedback training is the treatment of choice for medically refractory pelvic floor constipation, with some studies showing improvement in more than 70 percent of patients. Patients also learn to identify internal sensations associated with relaxation and long-term skills and exercises for use at home.

Although many centers are familiar with retraining techniques to improve pelvic floor dysfunction, few have the multidisciplinary expertise to teach patients with constipation how to appropriately coordinate abdominal and pelvic floor muscles during defecation, and how to use bowel management techniques, along with behavior modification, to relieve symptoms. Because pelvic floor dysfunction can be associated with psychological, sexual or physical abuse and other life stressors, psychological counseling is often included in the evaluation process.

CAUSES-

While exact causes are still being researched, doctors can link pelvic floor dysfunction to conditions or events that weaken the pelvic muscles or tear connective tissue:

• childbirth
• traumatic injury to the pelvic region
• obesity
• pelvic surgery
• nerve damage

The full causes of pelvic floor dysfunction are still unknown. But a few of the known factors include:

• Traumatic injuries to the pelvic area (like a car accident).
• Pregnancy.
• Overusing the pelvic muscles (like going to the bathroom too often or pushing too hard), eventually leading to poor muscle coordination.
• Pelvic surgery.
• Being overweight.
• Advancing age.

Does pregnancy cause pelvic floor dysfunction?

Pregnancy is a common cause of pelvic floor dysfunction. Often women get experience pelvic floor dysfunction after they give birth. Your pelvic floor muscles and tissues can become strained during pregnancy, especially if your labor was long or difficult.

Is pelvic floor dysfunction hereditary?

Pelvic floor dysfunction can run in your family. This is called a hereditary condition. Researchers are looking into a potential genetic cause of pelvic floor dysfunction.

SIGN AND SYMPTOM-

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There are a few well-known signs and symptoms that people experience when they have a problem with their pelvic floor muscles. The following list of signs and symptoms are common for people with weak pelvic floor muscles. Urinary dysfunction, erectile dysfunction, premature ejaculation, painful ejaculation, and chronic pelvic pain are some conditions that can be linked with weak pelvic floor muscles.

Men

• Constipation or bowel strains
• Ongoing pain in your pelvic region, genitals or rectum.
• A prolapse – may feel as though there is a bulge/ pressure in the rectum or a feeling of needing to use your bowels without actually needing to go.
• Accidentally leaking urine when you exercise, laugh, cough or sneeze.
• Feelings of urgency in needing to the bathroom, or not making it there in time.
• Frequent need to urinate.
• Difficulty emptying your bladder (discontinuous urination – stop and start multiple times) and bowels.
• The feeling of needing to have several bowel movements during a short period of time.
• Accidentally passing wind.
• Pain in your lower back that cannot be explained by other causes.
• Pain in the testicles, penis (referred pain from the pelvic floor) or pelvis during intercourse.
• Erectile dysfunction.
• Painful ejaculation.
• Premature ejaculation.

Erectile function requires contraction of the pelvic floor muscles to block blood from leaving the penis. When the muscles are weak the outflow of blood from the penis is not stopped resulting in erectile dysfunction. Through learning voluntary control of the pelvic floor muscles this can help prevent premature ejaculation by learning how to relax and contract the muscles. Urinary incontinence has a direct relationship with pelvic floor muscles. These muscles tighten as a closure mechanism for the tube from the bladder to the exit (urethra) and weakness of these muscles can cause leaking and dribbling.

Women

• Pain or numbness during intercourse.
• Ongoing pain in your pelvic region, genitals or rectum.
• A prolapse – may be felt as a bulge in the vagina (feeling or seeing a bulge or lump in or coming out of your vagina) or a feeling of heaviness, discomfort, pulling, dragging or dropping sensation.
• Accidentally leaking urine when you exercise, laugh, cough or sneeze (stress incontinence).
• Feelings of urgency in needing to the bathroom, or not making it there in time.
• Frequent need to urinate.
• Difficulty emptying your bladder (discontinuous urination – stop and start multiple times) and bowels.
• The feeling of needing to have several bowel movements during a short period of time.
• Constipation or bowel strains.
• Accidentally passing wind.
• Pain in your lower back that cannot be explained by other causes.

Prolapse is a common condition that can occur due to weak pelvic floor muscles in women. This occurs due to the womb, bladder, bowel or top of the vagina moving out of their normal positions and pushing into the vagina. This can cause pain and discomfort but can be improved with pelvic floor exercises and lifestyle changes . Urinary incontinence has a direct relationship with pelvic floor muscles. These muscles tighten as a closure mechanism for the tube from the bladder to the exit (urethra) and weakness of these muscles can cause leaking and dribbling.

Diagnosis

It’s important not to self-diagnose your symptoms because they may indicate more serious conditions.

To make a diagnosis, your doctor will review your medical history and observe your symptoms. After the initial consultation, your doctor will perform a physical evaluation to check for muscle spasms or knots. They will also check for muscle weakness.

To check for pelvic muscle control and pelvic muscle contractions, your doctor may perform an internal exam by placing a perineometer — a small, sensing device — into your rectum or vagina.

A less invasive option involves placing electrodes on your perineum, the area between the scrotum and anus or vagina and anus, to determine if you can contract and relax pelvic muscles.

Risk Factors

The chances of developing pelvic floor dysfunction among men and women have increased over the past few years. According to Berghmans et al. (2015) this trend is likely to continue. The incidence of pelvic floor problems is predicted to increase by 35% between 2010-2030.

These statistics emphasize the importance of expanding knowledge related to the risk factors for pelvic floor dysfunction. When assessing a patient, physiotherapists should focus on a detailed subjective examination including past medical history and presenting condition/complaint, as this may reveal potential predispositions. Goal-centered conversations with the patients can provide guidance in planning treatment, and where applicable, liaising with appropriate healthcare professionals to ensure a holistic approach to care.

Men

• Prostate surgery: In general, scientific literature examining pelvic floor dysfunction among males is limited. However, prostate surgery has been identified as a potential risk factor . Specific pelvic floor disorders include urinary incontinence and erectile dysfunction, which are quite common post-operatively (up to 89% of men suffer from these conditions). Individuals who undergo this procedure may experience disturbance in pelvic floor muscles (especially urinary sphincters) and altered nerve supply to the area. In prostatectomy, the prostate (partially regulating continence) is removed, increasing the probability of incontinence. The urinary sphincter nerves may occasionally be damaged during surgery due to their proximity to the prostate. As a result, the patients might later experience poor bladder control. Cavernous nerves, which are responsible for erectile function, may also be disrupted.

Women

• Age: Females experiencing menopause are at increased risk for developing pelvic organ prolapse by 21.1%. Wu et al. (2014)assessed the relationship between age and number of pelvic floor disorders. They revealed that with each decade, the risk dramatically increased. This is most likely due to the hormonal fluctuations which change the functioning of female urogenital structures. It includes weakening of the pelvic floor, as the muscle mass tends to decrease during aging.
• Direct injury to levator ani (ex. vaginal delivery, fall on groin) and loss of tone in pelvic muscles: This involves the levator ani changing position and widening of genital hiatus, causing the pelvic structures to rely on the connective tissue for support. Over time, this alteration results in weakening or tearing of the tissue/collagen and may contribute to the occurrence of pelvic organ prolapse.
• Pregnancy and the nature of childbirth: Overstretching/damaging of the pudendal nerve during vaginal birth, prolonged labour, instrumental (forceps) delivery,episiotomy (surgical procedure to increase opening in vagina), weight and number of children (parity) have also been known to increase the pelvic floor dysfunction risk by 4-16%. These findings have been supported through biomechanical models of the pelvic floor. The researchers revealed that during the crowning of the fetal head in a vaginal birth, there is a greater risk for the avulsion of levator ani leading to a potential prolapse. Additionally, an episiotomy has been suggested to increase anal lacerations and therefore, incontinence risk. Findings within the systematic review noted parity to be a risk factor for primary pelvic organ prolapse as well.
• Genetics:Women who have a positive family history of pelvic organ prolapse, are more likely to inherit the condition. Campneau et al. (2011)showed that the risk for pelvic organ prolapse increased 1.4 times in the genetically predisposed group, after controlling for vaginal deliveries, hysterectomy, and incontinence. Additionally, some evidence suggests that in females who are experiencing urinary incontinence, the connective tissue of the pelvic floor muscles may be genetically weak. Low socioeconomic status: This factor, especially among racial minorities, may contribute to poorer access to adequate information regarding pelvic floor dysfunction. The lack of resources create a challenge in recognizing the symptoms and importance of seeking professional support in a timely manner. Hartigan and Smith (2018), presented that women of poorer socioeconomic status scored lower on the incontinence quiz than their higher socioeconomic status counterparts. Consequently, there is a strong emphasis on public education to reduce the risk of pelvic floor dysfunction. Hysterectomy (surgical removal of the uterus): This procedure often damages and weakens the pelvic muscles. Therefore, it may be a predisposing factor for pelvic organ prolapse . Lukanovic and Drazic (2010) suggest that that the incidence of postoperative complications after hysterectomy, including urinary and fecal incontinence was significantly higher in the group who undertook the surgery for vaginal prolapse compared to a control group with no diagnosis of prolapse. Being middle-aged, as an additional factor to post-hysterectomy, increases the risk to 60% for developing urinary incontinence.

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TREATMENT-

The goal for treating pelvic floor dysfunction is to relax the pelvic floor muscles to make bowel movements easier and to provide more control.

Kegel exercises, or similar techniques that require you to contract your muscles, will not help this condition. While surgery is an option, there are less invasive treatment options available.

A common treatment for this condition is biofeedback. This technique allows your therapist to monitor how you relax or contract your pelvic muscles through special sensors. After observing your muscle activity, your therapist will tell you how to improve your coordination.

Other treatment options include:

• Medication. Your doctor may prescribe a muscle relaxant to help with pelvic floor dysfunction symptoms. The relaxants can prevent your muscles from contracting.
• Self-care. To reduce strain on your pelvic floor muscles, avoid pushing or straining when using the bathroom. Relaxation techniques such as yoga and stretching can also help to relax your pelvic floor muscles. Taking warm baths is another useful technique. Warm water improves blood circulation and relaxes the muscles.
• Surgery. If your pelvic floor dysfunction is the result of a rectal prolapse — a condition that causes the rectal tissue to fall into the anal opening — surgery will loosen the affected pelvic organs and cause them to relax.

Medical Management 

Pelvic floor dysfunction is a very treatable condition. Many ways exist to treat pelvic floor problems conservatively (non-surgical) and should generally be considered as the first-line option prior to more aggressive procedures such as surgery. Treatment will vary according to the nature of the condition or reason behind the dysfunction.

Pharmacological (Medication)

• Various drugs can be prescribed depending on the reason for the pelvic floor problems. Drug therapy is particularly common for urinary incontinence and will depend on the type of incontinence that your client is experiencing.
• The ageing process can lead to hormonal changes which can negatively impact the pelvic floor muscles and lead to increased laxity/stretching. Therefore, hormone replacement therapies for post-menopausal women can be used to manage or improve the symptoms.
• If your client has an over-active bladder or urge incontinence, there are medications to help relax the bladder and reduce the frequency of urination.
• Drug therapy is even more effective when used in combination with other strategies like pelvic floor exercises and lifestyle changes.

Surgical

• In some cases, when other strategies have been unsuccessful in achieving treatment goals, surgery may be the best treatment option. Depending on the specific condition, various procedures exist to address the problem.
• Incontinence and prolapse have multiple types of procedures to alter the pelvic structures or insert supports such as synthetic mesh slings, both in the goal of improving functions.
• For those who have a pelvic floor disorder, 1 in 9 will undergo surgery, however, there are risks associated with surgery as they don’t always succeed. Regarding synthetic mesh sling surgery, roughly 30% will require a second operation, and roughly 35% will need to be removed.
• Slightly less invasive options are also available, such as injections of Botox for urge incontinence or bulking agents to help reduce stress incontinence.

Physiotherapy Management

Education is the key and physiotherapists need to educate both male and female patients, on the function of the pelvic floor muscle. Assist the patient to understand the function of the pelvic floor muscle and how exercising this muscle can strengthen and reduce the risk of unwanted symptoms. This can help achieve that all important “buy in” and encourage the patient to be consistent with pelvic floor muscle training. However, explaining this can be tricky for any Physiotherapist due to the sensitivity of the subject! We have put together some tips that may be helpful to ensure a smooth, clear and lighthearted delivery!

• The Internal hammock – Try referring to the pelvic floor muscle as “ a hammock “ or a “trampoline “ which lies on the floor of the pelvis and supports organs such as the womb, bladder, bowel. This can make the function of the pelvic floor muscle easier to understand! And plus, who doesn’t want to learn about their very own internal trampoline, right?!
• Context is key! – Place emphasis on the strain that is put on the hammock or trampoline during everyday activities such as working, household duties, looking after family, exercising. Apply this to the patients’ life, by discussing their occupation, pastimes, and family situation and how the pelvic floor muscle or “trampoline “ is at risk of being overstretched as a result. This will help the patient to add context.
• Leaking waterworks?…. Time tighten up those taps! – Lack of bladder or bowel control can be a symptom of a weak pelvic floor and or a prolapse.This is an opportunity to empower the patient and show them they can still take control of their situation, through pelvic floor muscle training. Leaking, incontinence and increased urgency do not need to be tolerated! Ensure that the patient understands that there is an opportunity to tighten those taps right up! The only requirement is the right mindset and a top-notch spanner!
• Rome was not built in a day people! – It is important that physiotherapists stress that pelvic floor muscle training takes time, effort and consistency. Improvements in continence status and or stages of prolapse will not improve overnight and may take up to 3 weeks for any improvement to be felt. Be mindful of this and ensure that the patient is supported, as feelings of frustration may arise!
• If there is an issue, here is a tissue! – Physiotherapists deal with more than just muscles, we deal with emotions! It is important to be mindful of the impact that incontinence, leaking and prolapse can have on patient quality of life. Support, empathy, and compassion are an absolute necessity, to ensure the patient feels at ease. Listening to the patient and allowing them to tell you their concerns, hardships, and battles allow the patient to offload their worries and boost their feelings of self-efficacy as they begin their journey of self-management. Lending them your ear can be the greatest gift you can give.

The Correct Technique

Explaining a pelvic floor contraction is not an easy task! It is a difficult area, given the sensitivity of the subject that many patients feel uncomfortable with. Also, it is very confusing.  Medical and anatomical terminology can leave patients feeling lost or too embarrassed to ask questions. It is vital that exercising this complicated internal muscle is described in a simple but clear manner. Here are some tips that may be helpful, or if you find any nuggets of gold in this feel free to use!

The Female Contraction

• The pelvic floor muscle can be exercised in sitting standing or lying. Many patients seem to prefer sitting and feel the muscle is easier to engage in this position. Advise the patient to try out different positions to find what best suits
• In sitting, ensure both feet are placed on the floor and patient is relaxed and aware of their breathing. Encourage your patient to relax all muscles, including shoulders, abdominals, and glutes. Take a few moments to become aware of the breathing pattern.
• Ask the patient to imagine they are sitting on the toilet, having a wee. Ask them to then try and replicate the action of stopping the flow of urine mid-stream. Explain to them that this is a pelvic floor contraction involving the anterior muscles.
• Another handy example of a pelvic floor exercise is, again, ask the patient to imagine they are in a line waiting to pay for their shopping. They have been feeling bloated and the urge to pass wind has presented itself with full gusto! In order to hold that wind in it requires a contraction of the posterior pelvic floor muscles.
• Ask the patient to imagine they are sitting on the toilet. Ask them to then try and replicate the action of stopping the flow of urine mid-stream AND trying to stop themselves from passing wind at the same time. This involves a combined pelvic floor contraction of both anterior and posterior muscles.

Remember to remind your patients to never stop the flow of urine when actually going to the toilet as this may lead to difficulty in fully emptying the bladder in the long run! This is simply a visualization technique that may be helpful. Ensure to remind the patient that pelvic floor exercises can be done anytime anyplace, not only when sitting on the toilet!

EXERCISES-

The Knack Technique –   Get Involved People!

The knack technique can help to support pelvic floor health! Pressure builds up in the abdomen when lifting, exercising, coughing, sneezing laughing, lifting weights, turning to look out your rear window when driving. Basically, in pretty much everything we do! This creates a downward force or pressure on the pelvic floor muscles when can lead to our beloved internal “trampoline “ becoming stretched or laxThe knack technique involves contracting the pelvic floor muscle, before lifting, bending, sneezing, coughing, or any movement you can think of that will increase abdominal pressure. This is a supportive measure that can help maintain and support pelvic health.

The knack technique offers many benefits and can help patient’s become more involved in their pelvic health. Add context to this, go through patient activities of daily living, pastimes, family and suggest situations in which the knack technique can be useful. For example, lifting heavy shopping onto the kitchen counter, reminding the patient to contract the pelvic floor before lifting the bags, or contract the pelvic floor before lifting your 2-year-old teething toddler.

• Pelvic floor muscle training (PFMT) has been shown to be beneficial for both urinary incontinence and prolapse symptoms. A randomised control trial in adult women with pelvic floor dysfunctions suggests that using an intravaginal vibratory stimulus( IVVS) helps in improving the pelvic floor muscle strength as compared to intravaginal electrical stimulation (IVES). Findings from a review by Dumoulin et al. (2015) suggest that pelvic floor muscle training provides better outcomes compared to a control group in women with urinary incontinence. Li et al. (2016) found that those with pelvic organ prolapse undertaking pelvic floor muscle training had significantly greater improvements in subjective prolapse symptoms and objective prolapse severity compared to a control group.
• A study suggests that hypopressive exercises caused activation of the PFMs, abdominal, gluteal, and adductor muscles. 
• Pelvic floor training also seems to improve sexual function. The findings from a review by Ferreira et al. (2015) suggest that pelvic floor muscle training can improve sexual function or at least one sexual variable in women with pelvic floor dysfunction.
• Interesting findings from two RCTs also corroborate the evidence for pelvic floor muscle training. Alves et al. (2015) found that twelve group sessions of pelvic floor muscle training increased pelvic floor muscle contractility (p = 0.01) while decreasing urinary symptoms (p < 0.01) and anterior pelvic organ prolapse (p = 0.03). Hagen et al. (2014) found similar results with one to one sessions. They did note that longer-term investigations are required to strengthen the evidence.
• When prescribing a pelvic floor muscle training programme, adherence is important. According to a consensus statement by Dumoulin et al. (2015), a structured PFMT programme, an enthusiastic physiotherapist, audio prompts, use of established theories of behavior change, and user-consultations seem to increase adherence.
• The identified evidence fails to make any recommendations on the optimal dosage of pelvic floor muscle training.
• The NICE guidelines recommend a trial supervised PFMT programme for at least 3 months as first-line treatment for those with stress or urinary incontinence.At least 8 contractions three times a day.

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INTRODUCTION –

Nutrition counseling is a cornerstone of prenatal care for all women during pregnancy. A woman’s nutritional status not only influences her health, but also pregnancy outcomes and the health of her fetus-neonate. Physicians and other healthcare providers need to be cognizant of nutritional needs during pregnancy, as they differ significantly compared to non-pregnant populations. Furthermore, an individualized approach to nutritional counseling that considers a woman’s access to food, socioeconomic status, race-ethnicity and cultural food choices, and body mass index (BMI) is recommended. In addition, many of the recommendations are geared for uncomplicated pregnancies, so adjustments need to be made when complications, such as gestational diabetes, arise. A nutritionist or registered dietitian can help facilitate dietary counseling and interventions. In this chapter, the maternal physiological adaptations as well as macronutrient and micronutrient requirements during pregnancy and lactation will be reviewed. Other discussions on these topics will include multiple gestations, obesity in pregnancy, pregnancies after bariatric surgery, special diets, and common exposures during pregnancy.

Nutrition and lifestyle before and during pregnancy, lactation, infancy and early childhood have been shown to induce long-term effects on later health of the child, including the risk of common non-communicable diseases such as obesity, diabetes and cardiovascular disease . This phenomenon is referred to as “Early metabolic programming of long-term health and disease” or “Developmental origins of adult health and disease”. The available evidence is based on experimental studies in animals, observations from retrospective and prospective observational studies in human cohorts, increasingly from controlled intervention trials. To strengthen the evidence base, researchers from 36 institutions across the European Union, the United States, and Australia collaborate in the European Commission funded “EarlyNutrition Research Project”. This international multidisciplinary research collaboration explores how nutrition and metabolism during sensitive time periods of early developmental plasticity can have an impact on cytogenesis, organogenesis, metabolic and endocrine responses as well as epigenetic modification of gene expression, thereby modulating later health. Because of the global escalation in the prevalence of obesity, particular focus has been placed on the developmental origins of adiposity (i.e., body fatness), leading to increasing evidence that early life programming could contribute to the intergenerational transmission of obesity and associated health outcomes. The EarlyNutrition Project has received funding from the European Commission (FP7-289346-EARLY NUTRITION), with co-funding provided by the Australian National Health and Medical Research Council (NMHMRC), and project partners to achieve a total budget of 11.1 million Euro. The project is co-ordinated by the Dr. von Hauner Children’s Hospital, LMU – Ludwig-Maximilians-Universität Munich, Germany. The project characterises programming effects and their effect sizes through studying contemporary prospective longitudinal cohort studies, performing randomized controlled intervention trials during pregnancy and infancy, and exploring underlying mechanisms. In order to facilitate translational application, the partnership reviewed available evidence and developed recommendations for dietary practice for women before and during pregnancy and lactation, and for infants and young children, taking long-term health consequences into account. These recommendations are devised for women and children in affluent countries, such as people in Europe.

Background: A considerable body of evidence accumulated especially during the last decade, demonstrating that early nutrition and lifestyle have long-term effects on later health and disease (“developmental or metabolic programming”). Methods: Researchers involved in the European Union funded international EarlyNutrition research project consolidated the scientific evidence base and existing recommendations to formulate consensus recommendations on nutrition and lifestyle before and during pregnancy, during infancy and early childhood that take long-term health impact into account. Systematic reviews were performed on published dietary guidelines, standards and recommendations, with special attention to long-term health consequences. In addition, systematic reviews of published systematic reviews on nutritional interventions or exposures in pregnancy and in infants and young children aged up to 3 years that describe effects on subsequent overweight, obesity and body composition were performed. Experts developed consensus recommendations incorporating the wide-ranging expertise from additional 33 stakeholders. Findings: Most current recommendations for pregnant women, particularly obese women, and for young children do not take long-term health consequences of early nutrition into account, although the available evidence for relevant consequences of lifestyle, diet and growth patterns in early life on later health and disease risk is strong. Interpretation: We present updated recommendations for optimized nutrition before and during pregnancy, during lactation, infancy and toddlerhood, with special reference to later health outcomes. These recommendations are developed for affluent populations, such as women and children in Europe, and should contribute to the primary prevention of obesity and associated non-communicable diseases.

Improving Nutrition and Health for Pregnant and Lactating Women-

Maternal nutrition-

Nutrition for women in pre-pregnancy, pregnancy, and over the first two years of the child’s life is of utmost importance for the survival, health and development of mothers and their children. In pregnancy, requirements of energy, protein, and essential micronutrients (vitamins and minerals) are increased not only to maintain the mother’s own health, but to also support optimal physical and brain development in the foetus. Furthermore, nutrition reserves are built over pregnancy to produce breastmilk for the post-child birth phase. Deficiencies of energy, protein, iron, calcium, iodine, vitamin A and folic acid during pregnancy predispose mothers to maternal complications and even mortality. These also contribute to foetal birth defects, low birth weight, restricted physical and mental potential, and foetal or newborn mortality.

Exclusive breastfeeding is recommended for infants 0-6 months of age to meet all their nutrition needs for optimal growth, and to protect them from infection. This should be followed by continued breastfeeding alongside appropriate complementary feeding until the child reaches 2 years of age. To sustain the production of adequate quantity and nutritional quality of breastmilk, lactating women have higher requirements of energy, protein, and other micronutrients. Poor maternal nutrition over this period risks depletion of the mother’s own nutrient stores and health, and harms the nutrition and health of the growing child . Addressing nutritional needs of pregnant and lactating women is now entrenched within the Sustainable Development Goals. By scaling up efforts to achieve this target, progress will also be accelerated on the targets on maternal and child mortality and health.

Maternal nutrition and health-

The impact of poor nutrition on maternal health and survival is indisputable. Anaemia, which results from deficiencies of nutrients such as iron and folic acid is an important risk factor for haemorrhage; a leading cause of maternal mortality. Calcium deficiency during pregnancy also increases the risk of pre-eclampsia, another cause of maternal mortality . Improving nutrition alongside good antenatal care can reduce these numbers significantly. Globally 52% of maternal deaths are attributable to haemorrhage, sepsis, and hypertensive disorders; 28% to non-obstetric causes; 8% to unsafe abortion . Infection during pregnancy can deteriorate a mother’s nutritional and health status, and impact foetal development. Maternal infections before or during childbirth are known to be associated with around 1 million new-born deaths each year, and contribute to about 10% of the global burden of maternal mortality. Malnutrition, is one of the main factors increasing the risk of such life-threatening infections through its role in decreasing immunity and delaying recovery .

PREGNANCY

Energy Expenditure during Pregnancy

Caloric intake should increase by approximately 300 kcal/day during pregnancy. This value is derived from an estimate of 80,000 kcal needed to support a full-term pregnancy and accounts not only for increased maternal and fetal metabolism but for fetal and placental growth. Dividing the gross energy cost by the mean pregnancy duration (250 days after the first month) yields the 300 kcal/day estimate for the entire pregnancy. However, energy requirements are generally the same as non-pregnant women in the first trimester and then increase in the second trimester, estimated at 340 kcal and 452 kcal per day in the second and third trimesters, respectively. Furthermore, energy requirements vary significantly depending on a woman’s age, BMI, and activity level. Caloric intake should therefore be individualized based on these factors.

Laboratory Testing during Pregnancy

Physiological changes during pregnancy alter the normal ranges of several laboratory values. Both total red blood cell mass and plasma volume increase, but plasma volume increases to a greater extent resulting in hemodilution and anemia during pregnancy. Consequently, a hemoglobin <10.5 g/dl or a hematocrit <32% is considered anemic during the second trimeste. Serum total protein and albumin also decrease by approximately 30% compared to non-pregnant values. Additionally, because estrogen increases the hepatic production of certain proteins, there is greater protein binding of corticosteroids, sex steroids, thyroid hormones, and vitamin D during pregnancy, resulting in lower free levels.

Nutrients

Macronutrients

Recommended protein intake during pregnancy is 60g/day, which represents an increase from 46g/d in non-pregnant states. In other words, this increase reflects a change to 1.1g of protein/kg/day during pregnancy from 0.8g of protein/kg/day for non-pregnant states. Carbohydrates should comprise 45-64% of daily calories and this includes approximately 6-9 servings of whole grain daily. Total fat intake should comprise 20-35% of daily calories, similar to non-pregnant women.

Micronutrients

The recommendations for daily micronutrient intake for a pregnant woman are determined by the “Recommended Dietary Allowances” or RDA data. In general, these RDA refer to the levels of intake of essential nutrients that are judged by the Food and Nutrition Board of the Institute of Medicine (IOM) to be adequate to meet the known nutrient needs of practically all healthy persons. The RDA have been modified for pregnant women. shows the dietary allowances for most vitamins and minerals during pregnancy and they are reviewed in further detail below.

A daily prenatal multivitamin is generally recommended before conception and during pregnancy. describes the typical composition of a prenatal vitamin. The critical difference compared to other multivitamins is the folic acid dose, which is necessary to support rapid cell growth, cell replication, cell division, and nucleotide synthesis for fetal and placental development. While there is data to support additional folic acid and iron supplementation during pregnancy, there is no high quality evidence demonstrating that all women require the increased levels of nutrients in a prenatal vitamin.

Gestational Weight Gain

Pregnancy has traditionally been considered a time for weight gain, not weight loss. The obligatory weight gain during pregnancy is approximately 8 kg which accounts for the fetus, the placenta, amniotic fluid volume, and adaptations to maternal tissues (e.g., uterus, breast, blood volume). A weight gain less than this amount implies that existing maternal adipose and protein stores would be mobilized in order to support the pregnancy. Metabolic changes of women who lose weight during pregnancy are not well-described, but ketonemia, increased urinary nitrogen excretion, and decreased gluconeogenic amino acid production result after a period of fasting during pregnancy. Pregnancy is often considered a time of “accelerated starvation” due to the increase in insulin resistance, with an increased risk for developing ketonuria and ketonemia. This physiologic change is important to consider in the setting of weight loss during pregnancy because maternal ketonemia or ketonuria may subsequently be associated with abnormal fetal growth or later neurocognitive developmen.

Obesity

The World Health Organization and the National Institutes of Health define normal weight as a BMI of 18.5–24.9 kg/m², overweight as a BMI of 25–29.9 kg/m², and obesity as a BMI of 30 kg/m² or greater. Obesity is further categorized by BMI into Class I (30–34.9 kg/m²), Class II (35–39.9 kg/m²), and Class III or extreme obesity (≥ 40 kg/m²).Trends in adult weight over the past couple of decades highlight the escalating role that obesity plays in women’s health; 31.8% of reproductive age women (20-39 years) had obesity in 2011-2012.Women with a higher pre-pregnancy BMI have a greater risk for adverse perinatal outcomes. These include both maternal complications such as gestational diabetes, pregnancy-related hypertension, and cesarean deliveries along with adverse fetal effects such as birth defects, stillbirth, and abnormal fetal growth.As such, weight loss prior to pregnancy is strongly recommended in order to reduce the risk of these complications.

Pregnancy after bariatric surgery

Pregnancy after bariatric surgery is not uncommon as fertility often improves after a bariatric surgery procedure.Given that bariatric procedures can create deficiencies of micro- and macronutrients, a pregnancy occurring after a bariatric surgery procedure requires particular attention to nutritional status. As stated previously, requirements for calories, vitamins, and minerals increase during pregnancy, so nutritional deficiencies in the bariatric surgery patient can be exacerbated during pregnancy. The most common deficiencies that occur after bariatric surgery are vitamin B₁₂, folate, and iron.Because malabsorptive procedures (e.g., Roux-en-y gastric bypass [RYGB], biliopancreatic diversion) have a higher risk for nutritional deficiencies, closer surveillance in pregnancies that occur after these types of surgeries is appropriate. However, derangements in nutrients can also occur after restrictive-type procedures (e.g., laparoscopic adjustable gastric banding), so it may be reasonable to screen all women who are pregnant post-bariatric surgery for nutritional deficiencies. Guidelines for screening and management of nutritional deficiencies during pregnancy are adapted from those designed for non-pregnant states and include laboratory testing once a trimester or every 3 months if the levels are normal .Iron deficiency anemia is frequently a long-term complication of bariatric surgery, occurring in 6% to 50% of patients after RYGB. In pregnancies after bariatric surgery, iron deficiency anemia can be diagnosed in the usual manner with a low mean corpuscular volume, and abnormal iron studies (e.g., low serum iron, high total iron-binding capacity, and a low serum ferritin) keeping in mind the physiologic anemia that occurs during pregnancy . Treatment of vitamin and mineral deficiencies during pregnancy, in terms of dose and duration, is similar to that of non-pregnant states.

Vegetarians

There are varying types of vegetarian diets such as ovolactovegetarian (includes dairy and egg products), ovovegetarian (includes eggs), lactovegetarian (includes dairy products), and vegan (excludes eggs, dairy, and any other animal products). Alternative protein sources for these women include beans, peas, soy, nuts, nut butter, and milk and egg products. Minerals that may be deficient in their diets include iron, calcium, zinc, and vitamin B₁₂. Laboratory testing for these specific nutrients may be indicated.

Eating disorders

For women with either a history of or current eating disorder (e.g., anorexia nervosa, bulimia), additional questions regarding their weight should be asked including how they feel about weight gain, being weighed at every prenatal visit (which is customary in prenatal care practices in the United States), and the ongoing changes in their body.With respect to weighing, a woman’s preference about weighing (i.e., whether or not she prefers to see the numbers) should be assessed and documented in the chart. Counseling on gestational weight gain goals is still important for these women as weight influences the growth and development of the fetus. Similar to management prior to pregnancy, a collaborative team of experts in eating disorders should continue to manage and treat these women during the pregnancy.

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LACTATION

Physiology and Production

Breastfeeding and breast milk are the global standard for infant feeding. The World Health Organization, the U.S. Surgeon General, the American Academy of Pediatrics, the American Congress of Obstetricians and Gynecologists, the American Academy of Family Practice, and the Academy of Breastfeeding Medicine all support this statement. The American Academy of Pediatrics further recommends exclusive breastfeeding for the first 6 months and breastfeeding at least through the first year of life.Similar to pregnancy, energy and nutritional requirements also differ during lactation and breastfeeding.

Women who breastfeed require approximately 500 additional kcal/day beyond what is recommended for non-pregnant women.The estimate is derived from the mean volume of breast milk produced per day (mean 780 mL, range 450-1200 mL) and the energy content of milk (67 kcal/100 mL).During pregnancy, most women store an extra 2 to 5 kg (19,000 to 48,000 kcal) in tissue, mainly as fat, in physiologic preparation for lactation. If women do not consume the extra calories, then body stores are used to maintain lactation. It is not unusual for lactating women to lose 0.5-1.0 kg/month after the first postpartum month.

Special Considerations

Multiple Gestations

Approximately 40-90% of mothers of twins initiate breastfeeding.⁸⁷ The production of milk is primarily determined by infant demand rather than the maternal capacity to lactate. As such, for women attempting to breastfeed twins and triplets, the supply will meet the demand. Continuation of micronutrient supplementations given antenatally in the form of a prenatal vitamin is appropriate for women who are breastfeeding twins. Twins can breastfeed either simultaneously or separately.

Special Considerations

Multiple Gestations

Approximately 40-90% of mothers of twins initiate breastfeeding.The production of milk is primarily determined by infant demand rather than the maternal capacity to lactate. As such, for women attempting to breastfeed twins and triplets, the supply will meet the demand. Continuation of micronutrient supplementations given antenatally in the form of a prenatal vitamin is appropriate for women who are breastfeeding twins. Twins can breastfeed either simultaneously or separately.

Approximately 40-90% of mothers of twins initiate breastfeeding. The production of milk is primarily determined by infant demand rather than the maternal capacity to lactate. As such, for women attempting to breastfeed twins and triplets, the supply will meet the demand. Continuation of micronutrient supplementations given antenatally in the form of a prenatal vitamin is appropriate for women who are breastfeeding twins. Twins can breastfeed either simultaneously or separately.

Obesity

Several studies have demonstrated that women with obesity have decreased rates of initiating breastfeeding and breastfeed for shorter durations compared to normal weight women.Biological (i.e. delayed lactation), psychological (i.e., embarrassment related to body size and difficulty in breastfeeding discreetly), mechanical (i.e., larger breasts and nipples that create difficulties with latching), and medical (i.e., cesarean deliveries, diabetes, thyroid dysfunction) factors have been theorized to explain these findings, but the exact etiology is likely a combination of factors. To combat this trend and increase the likelihood that women with obesity attain their breastfeeding goals, they need additional support and encouragement to breastfeed, including assistance with appropriate latching techniques and demonstration of appropriate infant positions, to aid with initiation and continuation of lactation.

Bariatric surgery

Women who have had bariatric surgery are also advised to follow the recommendation of breastfeeding for at least 6 months. Laboratory evaluation of micronutrient levels, as described in for pregnant women, is also recommended for breastfeeding women after bariatric surgery, with one group suggesting they be tested as frequently as every 3 months. The infant’s provider also should be aware of the mother’s history of bariatric surgery as well as any of her specific dietary restrictions or identified nutrient deficiencies. For women who have a gastric banding procedure, one recommendation is to keep the band deflated until the successful establishment of breastfeeding. Though few studies have evaluated the nutritional content of breast milk produced by lactating women after bariatric surgery, it is likely similar to other women. While infants who are born to women with obesity have a higher rate of early childhood obesity, this may be offset by the reduced risk of early childhood obesity in infants who are predominantly breastfed.

Vegetarians

Recommended dietary guidelines for vegetarians during lactation are lacking. Vitamin D supplements are recommended for women who do not drink milk or other food fortified with vitamin D. A vitamin B₁₂ supplement (2.6 μg/d) is also recommended for women who consume ovolactovegetarian and vegan diets. Another recommendation is to consume 1200-1500 mg/day of calcium because of the possible decreased intake and absorption from a plant-based diet.The FDA recommends similar precautions regarding avoiding higher mercury fish during lactation. Adverse neonatal effects have not been demonstrated with ordinary maternal fish consumption during breastfeeding.

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INTRODUCTION-

An abscess in the brain of an otherwise healthy person is usually caused by bacterial infection. Fungal brain abscesses tend to occur in people with weakened immune systems. The infection will cause your brain to swell from the collection of pus and dead cells that forms.

A brain abscess forms when fungi, viruses, or bacteria reach your brain through a wound in your head or an infection somewhere else in your body. According to the Children’s Hospital of Wisconsin, infections from other parts of the body account for between 20 and 50 percent of all brain abscess cases. Heart and lung infections are among the most common causes of brain abscesses. However, brain abscesses can also begin from an ear or sinus infection, or even an abscessed tooth.

See your doctor right away if you think you may have a brain abscess. You’ll need the appropriate treatment to prevent any brain damage from the swelling.

Intracranial abscesses are uncommon, serious, life-threatening infections. They include brain abscess and subdural or extradural empyema and are classified according to the anatomical location or the etiologic agent. The term brain abscess is used in this article to represent all types of intracranial abscesses.

Intracranial abscesses can originate from infection of contiguous structures (eg, otitis media, dental infection, mastoiditis, sinusitis) secondary to hematogenous spread from a remote site (especially in patients with cyanotic congenital heart disease), after skull trauma or surgery, and, rarely, following meningitis. In at least 15% of cases, no source can be identified.

A brain abscess is a collection of pus that develops in response to an infection or trauma. It remains a serious and potentially life-threatening condition.

In the past, a brain abscess was “invariably fatal,” but researchers writing in 2014 noted that progress in diagnosis and treatment have significantly increased the chances of survival.

The effects vary, depending on the size of the abscess and where it forms in the brain.

Between 1,500 and 2,500 cases occur each year in the United States. Brain abscesses are most likely to affect adult men aged under 30 years. Among children, they most commonly develop in those aged 4–7 years. Newborns are also at risk.

Vaccination programs have reduced the incidence of brain abscesses in young children.

CAUSES-

A brain abscess is most likely to result from a bacterial or fungal infection in some part of the brain. Parasites can also cause an abscess.

When the bacteria, fungi, or parasites infect part of the brain, inflammation and swelling occur. In these cases, the abscess will consist of infected brain cells, active and dead white blood cells, and the organisms that cause the problem.

As the cells accumulate, a wall or membrane develops around the abscess. This helps to isolate the infection and keep it from spreading to healthy tissue.

If an abscess swells, it puts increasing pressure on surrounding brain tissue.

The skull is not flexible, and it cannot expand. The pressure from the abscess can block blood vessels, preventing oxygen from reaching the brain, and this results in damage or destruction of delicate brain tissue.

here are 3 main ways a brain abscess can develop. These are:

• an infection in another part of the skull – such as an ear infection, sinusitis or dental abscess, which can spread directly into the brain
• an infection in another part of the body – for example, the infection that causes pneumonia spreading into the brain via the blood
• trauma, such as a severe head injury – that cracks open the skull, allowing bacteria or fungi to enter the brain

However, in some cases, the source of the infection remains unknown.

SYMPTOM-

Symptoms usually develop slowly over several weeks, but they can also come on suddenly. Symptoms you should watch for are:

• differences in mental processes, such as increased confusion, decreased responsiveness, and irritability
• decreased speech
• decreased sensation
• decreased movement due to loss of muscle function
• changes in vision
• changes in personality or behavior
• vomiting
• fever
• chills
• neck stiffness, especially when it occurs with fevers and chills
• sensitivity to light

In babies and young children, most of the symptoms are similar. However, your child may show other symptoms of a brain abscess. The soft spot on top of your baby’s head, called the fontanelle, may be swollen or bulging. Other symptoms in your child can include:

• projectile vomiting
• high-pitched crying
• spasticity in the limbs

The signs and symptoms of a brain abscess are as follows:

• a headache (69–70 percent of cases)
• a fever (45–53 percent)
• seizures (25–35 percent)
• nausea and vomiting (40 percent)

A seizure may be the first sign of an abscess. Nausea and vomiting tend to occur as pressure builds inside the brain.

Pain usually starts on the side of the abscess, and it may begin slowly or suddenly.

Changes in mental status occur in 65 percent of cases, and they may lead to:

• confusion
• drowsiness and lethargy
• irritability
• poor mental focus
• poor responsiveness
• slow thought processes
• coma (possibly)

Neurologic difficulties affect 50–65 percent of people with brain abscesses. These issues often follow a headache, appearing within days or weeks, and they can include:

• muscle weakness
• weakness or paralysis on one side of the body
• speech problems, such as slurred speech
• poor coordination

Other symptoms may include:

• a stiff neck, back, or shoulders
• blurred, double, or graying vision

The symptoms of a brain abscess result from a combination of infection, brain tissue damage, and pressure on the brain, as the abscess grows to take up more space.

If the headache suddenly becomes worse, it may mean that the abscess has burst.

In two-thirds of cases, symptoms are present for as long as 2 weeks. On average, doctors diagnose the issue 8 days after symptoms start.

When to get medical advice

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Any symptoms that suggest a problem with the brain and nervous system should be treated as a medical emergency. These include:

• slurred speech
• muscle weakness or paralysis
• seizures occurring in a person with no previous history of seizures

If you or someone you know experiences any of these symptoms, phone 999 immediately and ask for an ambulance.

Any symptoms that suggest a worsening infection, such as a high temperature or being sick, should be reported to your GP immediately.

DIAGNOSIS-

Many of these symptoms closely resemble other diseases or health problems. Talk to your doctor immediately if you develop any of the symptoms. You’ll likely need a neurological exam. This exam can reveal any increased pressure within the brain, which can occur from swelling. CT and MRI scans can also be used to diagnose a brain abscess.

In some cases, your doctor may need to perform a lumbar puncture, or spinal tap. This involves the removal of a small amount of cerebral spinal fluid to test for any problems other than an infection. A lumbar puncture will not be performed if any significant brain swelling is suspected, as it can temporarily worsen the pressure inside the head. This is to avoid the risk of brain hematoma, or a ruptured blood vessel in the brain.

To diagnose a brain abscess, the doctor will evaluate signs and symptoms and look at the patient’s recent medical and travel histories.

They will need to know whether the individual:

• has had an infection recently
• has a weakened immune system

Symptoms can be similar to those of other illnesses and conditions, so it may take time to confirm a diagnosis. The diagnosis will be more straightforward if the doctor can pinpoint exactly when symptoms started and how they progressed.

Tests may include:

• a blood test to check for high levels of white blood cells, which can indicate an infection
• imaging scans, such as an MRI or a CT scan, in which an abscess will show up as one or more spots
• a CT-guided aspiration, a type of needle biopsy, which involves taking a sample of pus for analysis

The number of fatalities from brain abscesses has fallen in recent decades, due to the increasingly routine use of CT and MRI scans in detection.

How infection enters the brain

Brain infections are fairly uncommon for several reasons.

One reason involves the blood-brain barrier, a protective network of blood vessels and cells. It blocks certain components from the blood that flows to the brain, but it allows others to pass through.

Sometimes, an infection can get through the blood-brain barrier. This can happen when inflammation damages the barrier, leading to gaps.

The infection enters the brain through three main routes.

It may:

• come through the blood from an infection in another part of the body
• spread from a nearby site, such as the ear
• result from a traumatic injury or surgery

Infection from another area of the body

If an infection occurs somewhere else in the body, the infectious organisms can travel through the bloodstream, bypass the blood-brain barrier, and enter and infect the brain.

Between 9 and 43 percent of abscesses result from pathogens that traveled from another part of the body.

Many bacterial brain abscesses stem from a lesion somewhere else in the body. It is crucial to find that primary lesion, or there may be a repeat infection in the future.

A person with a weakened immune system has a higher risk of developing a brain abscess from a bloodborne infection.

A person may have a weakened immune system if they:

• have HIV
• have AIDS
• are infants under the age of 6 months
• are receiving chemotherapy
• are using long-term steroid medication
• have had an organ transplant and take immunosuppressant drugs to prevent organ rejection

The most common infections known to cause brain abscesses are:

• endocarditis, an infection of the heart valve
• pneumonia, bronchiectasis, and other lung infections and conditions
• abdominal infections, such as peritonitis, an inflammation of the inner wall of the abdomen and pelvis
• cystitis, or inflammation of the bladder, and other pelvic infections

Direct contagion-

An infection can spread from a nearby area, and this accounts for 14–58 percent of brain abscesses.

If an infection starts inside the skull, for example in the nose or the ear, it can spread to the brain.

Infections that can trigger a brain abscess include:

• otitis media, or a middle ear infection
• sinusitis
• mastoiditis, an infection of the bone behind the ear

The location of the abscess may depend on the site and type of the original infection.

Direct trauma

A brain abscess can result from trauma, such as from neurological surgery or a penetrating brain injury.

An abscess can result from:

• a blow to the head that causes a compound skull fracture, in which fragments of bone are pushed into the brain
• the presence of a foreign body, such as a bullet, if someone does not remove it
• a complication of surgery, in rare cases

What are the risk factors?

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Nearly anyone can get a brain abscess, but certain groups of people are at a higher risk than others. Some diseases, disorders, and conditions that raise your risk include:

• a compromised immune system due to HIV or AIDS
• cancer and other chronic illnesses
• congenital heart disease
• major head injury or skull fracture
• meningitis
• immunosuppressant drugs, such as those used in chemotherapy
• chronic sinus or middle ear infections

Certain birth defects allow infections to reach the brain more easily through the teeth and intestines. One example of this is tetralogy of Fallot, which is a heart defect.

TREATMENT-

Treatment for a brain abscess usually involves a combination of medicines and surgery, depending on the size and number of brain abscesses.

A brain abscess is a medical emergency, so you’ll need treatment in hospital until your condition is stable.

Treatment with medicines often begins before a diagnosis is confirmed to reduce the risk of complications.

Medicines

In some cases, it may be possible to treat an abscess with medicine alone, or surgery may be too risky.

Medicines are recommended over surgery if you have:

• several abscesses
• a small abscess (less than 2cm)
• an abscess deep inside the brain
• meningitis (an infection of the protective membranes that surround the brain) as well as an abscess
• hydrocephalus (a build-up of fluid on the brain)

You’ll normally be given antibiotics or antifungal medicine through a drip, directly into a vein. Doctors will aim to treat the abscess and the original infection that caused it.

Surgery

If the abscess is larger than 2cm, it’s usually necessary to drain the pus out of the abscess. However, you’ll still need a course of antibiotics after surgery.

There are 2 surgical techniques for treating a brain abscess:

• simple aspiration
• craniotomy

Simple aspiration involves using a CT scan to locate the abscess and then drilling a small hole known as a “burr hole” into the skull. The pus is drained and the hole sealed.

A simple aspiration takes around an hour to complete.

Open aspiration and excisions are usually carried out using a surgical procedure known as a craniotomy.

Craniotomy

A craniotomy may be recommended if an abscess does not respond to aspiration or reoccurs at a later date.

During a craniotomy, the surgeon shaves a small section of your hair and removes a small piece of your skull bone (a bone flap) to gain access to your brain.

The abscess is then drained of pus or totally removed. CT-guidance may be used during the operation, to allow the surgeon to more accurately locate the exact position of the abscess.

Once the abscess has been treated, the bone is replaced. The operation usually takes around 3 hours, which includes recovery from general anaesthetic, where you’re put to sleep.

Complications of a craniotomy

As with all surgery, a craniotomy carries risks, but serious complications are uncommon.

Possible complications of a craniotomy may include: 

• swelling and bruising around your face – which is common after a craniotomy and should lessen after the operation
• headaches – these are common after a craniotomy and may last several months, but should eventually settle down
• a blood clot in the brain – further surgery may be required to remove it
• stiff jaw – the surgeon may need to make a small cut to a muscle that helps with chewing, which will heal but can become stiff for a few months; exercising the muscle by regularly chewing sugar-free gum should help relieve the stiffness
• movement of the bone flap – the bone flap in your skull may feel like it moves and you may experience a clicking sensation; this can feel strange, but it is not dangerous and will stop as the skull heals

The site of the cut (incision) in your skull can become infected, although this is uncommon. You’re usually given antibiotics around the time of your operation to prevent infection.

Recovering from surgery

Once your brain abscess has been treated, you’ll probably stay in hospital for several weeks so your body can be supported while you recover.

You’ll also receive a number of CT scans, to make sure the brain abscess has been completely removed.

Most people need a further 6 to 12 weeks rest at home before they’re fit enough to return to work or full-time education.

After treatment for a brain abscess, avoid any contact sport where there’s a risk of injury to the skull, such as boxing, rugby or football.

Advice for drivers

If you’ve had brain surgery and you hold a driving licence, you’re legally required to inform the Driver & Vehicle Licensing Agency (DVLA).

It’s likely that the DVLA will suspend your driving licence due to your increased risk of having a seizure. Your licence will only be returned once your GP or surgeon confirms it’s safe for you to drive.

For most people, this is likely to be 12 months after surgery without having any seizures during this time.

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INTRODUCTION-

Cerebral edema is also known as brain swelling. It’s a life-threatening condition that causes fluid to develop in the brain.

This fluid increases the pressure inside of the skull — more commonly referred to as intracranial pressure (ICP). Increased ICP can reduce brain blood flow and decrease the oxygen your brain receives. The brain needs an uninterrupted flow of oxygen to function properly.

Swelling is the body’s response to injury. It can sometimes be treated with medication and rest.

Brain swelling can be very difficult to treat. It can also cause irreversible damage. The swelling can occur throughout the brain or in certain areas. Left untreated, cerebral edema can be fatal.

Cerebral edema, or brain swelling, is an increase of pressure in your head that may disrupt the blood-brain barrier. It is the body’s way of responding to trauma, stroke, or infection. Because the brain is encased in a rigid skull, increased intracranial pressure, or ICP, can prevent oxygen-rich blood from flowing to the brain, block fluids from leaving the brain, and even damage or kill brain cells.

A person suffering from cerebral edema may experience uncomfortable symptoms, like a headache, nausea, memory loss, or loss of consciousness.

Cerebral edema is a life-threatening condition that can cause permanent brain damage or death if not treated quickly.

Swelling — also called edema — is the body’s response to many types of injury. It can result from overuse or infection. Usually, swelling happens quickly and is simple to treat with some combination of rest, ice, elevation, medication, or removal of excess fluid.

Your brain can also swell as a result of injury, illness, or other reasons. Brain swelling, though, can quickly cause serious problems — including death. It’s also usually more difficult to treat. As your body’s master control system, the brain is critical to overall function. Yet, the thick, bony skull that snugly protects this vital organ provides little room for the brain to swell.

Brain swelling goes by many names:

• Brain edema
• Elevated intracranial pressure
• Cerebral edema

Swelling can occur in specific locations or throughout the brain. It depends on the cause. Wherever it occurs, brain swelling increases pressure inside the skull. That’s known as intracranial pressure, or ICP. This pressure can prevent blood from flowing to your brain, which deprives it of the oxygen it needs to function. Swelling can also block other fluids from leaving your brain, making the swelling even worse. Damage or death of brain cells may result.

TYPES-

There are five main types of cerebral edema. The type a person may be suffering from is dependent on the cause of injury.

• Cytotoxic This type of cerebral edema is the most common form of cerebral edema, and it results from an accumulation of sodium and water within the cells that leads to cellular failure. The main causes of this type of edema include traumatic brain injury, metabolic disease, infections like encephalitis or meningitis, or the ingestion of chemicals like methanol or ecstasy.
• Vasogenic If you have a stroke, there’s a chance your brain could swell due to a blood clot or a lack of oxygen. This causes a disruption of the blood-brain barrier that allows fluid to leak and pressure to build inside the brain. This form of cerebral edema is most commonly seen in people with brain tumors, but it can also be caused by too much carbon dioxide in the blood, metabolic disease, lead toxicity, and high altitude cerebral edema (HACE).
• Interstitial The main cause of this type of edema is obstructive hydrocephalus, which is the accumulation of cerebrospinal fluid from an abnormal widening of the ventricles that increases pressure in the brain. Obstructive hydrocephalus results from a genetic defect, developmental disorder, meningitis, tumor, traumatic brain injury, or hemorrhage.
• Hydrostatic Hydrostatic edema is the accumulation of interstitial fluid, which is the fluid in between the small, narrow spaces between tissues. Chronic venous obstruction or heart failure can elevate capillary hydrostatic pressure and cause the brain to swell.
• Osmotic “Cells have water inside and outside, and water can pass through their semipermeable membranes,” says Ram Balu, MD, PhD, an assistant professor of neurology at the University of Pennsylvania in Philadelphia. “This process is called osmosis. Sometimes, there can be a buildup of electrolytes inside the cell, and this causes a high concentration of water to move into the cells.” This imbalance osmolality is usually caused by serum osmolality from inappropriate antidiuretic hormone (SIADH) secretion or a TBI and leads to abnormal pressure, fluid, and swelling in the brain.

CAUSES-

Head trauma, infections, and a number of other neurological conditions can cause the brain to swell as pressure increases and compresses brain tissue. The typical causes of brain swelling include:

• Traumatic Brain Injury (TBI) A TBI is a blow to the head that can result in bleeding, bruising, or swelling of the brain. Common causes of TBI include falls, car crashes, sports, domestic violence, or combat injuries. The increase in intracranial pressure can cause brain tissue to swell.
• Infections A few different types of infections can result in brain swelling, including encephalitis and meningitis. Encephalitis is inflammation of the brain typically caused by a viral infection. It can lead to headache, fever, loss of consciousness, seizures, and more. Meningitis is an infection of the meninges that surround the brain and spinal cord. Typical causes include viral, bacterial, parasitic, or fungal infections.

Illness caused by an infectious organism such as a virus or bacterium can lead to brain swelling. Examples of these illnesses include:

• Meningitis: This is an infection in which the covering of the brain becomes inflamed. It can be caused by bacteria, viruses, other organisms, and some medications.
• Encephalitis: This is an infection in which the brain itself becomes inflamed. It is most often caused by a group of viruses and is spread usually through insect bites. A similar condition is called encephalopathy, which is due to Reye’s syndrome.
• Toxoplasmosis: This infection is caused by a parasite. Toxoplasmosis most often affects fetuses, young infants, and people with damaged immune systems.
• Subdural empyema: Subdural empyema refers to an area of the brain becoming abscessed or filled with pus, usually after another illness such as meningitis or a sinus infection. The infection can spread quickly, causing swelling and blocking other fluid from leaving the brain.

• Tumors A brain tumor is an abnormal growth of cells inside the brain or skull. It can compress or displace brain tissue or block cerebrospinal fluid, which can increase pressure and cause swelling.
• Stroke About 80 percent of strokes are ischemic strokes caused by blockages in the arteries in the brain, which in turn prevent oxygenated blood from reaching brain cells. Injured brain cells typically swell and can block the drainage of cerebrospinal fluid from the brain, driving pressure even higher.
• Brain Hemorrhage An intracranial hemorrhage is bleeding within or around the brain, and a hemorrhagic stroke involves death of brain cells as a result of a ruptured or torn blood vessel in the brain. Both of these conditions can cause brain swelling.
• High Altitudes You can develop high-altitude cerebral edema (HACE) about two days after from climbing above 4,000 meters (13,123 feet). This type of brain swelling occurs alongside acute mountain sickness (AMS), ataxia (loss of control of body movements), fatigue, and altered mental state. It can progress to a coma or death within 24 hours if not treated.

SYMPTOM-

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Cerebral edema can be difficult for doctors to diagnose without proper tests and a thorough evaluation.

There are some symptoms to look for after an injury or infection that could indicate swelling. Some indications of cerebral edema include:

• headache
• dizziness
• nausea
• lack of coordination
• numbness

In more severe cases of cerebral edema, you may experience symptoms including:

• mood changes
• memory loss
• difficulty speaking
• incontinence
• change in consciousness
• seizures
• weakness

DIAGNOSIS-

The steps used by your doctor to diagnose brain swelling depend on the symptoms and the suspected cause. Common exams and tests used in the diagnosis include:

• Head and neck exam
• Neurologic exam
• CT scan of the head to identify the extent and location of the swelling
• MRI of the head to identify the extent and location of the swelling
• Blood tests to check for causes of the swelling

PREVENTION-

Preventing cerebral edema involves taking measures to protect your head. Some options include:

• Using a helmet during sports or physical activities to prevent unexpected brain injury
• Controlling your blood pressure and cholesterol to prevent heart disease and stroke
• Wearing seat belts when traveling in a vehicle
• Slowly ascending to high elevations to avoid HACE
• Avoiding smoking to reduce the oxidative and inflammatory risk for stroke. (15)
• Monitoring your blood pressure and cholesterol to reduce your risk of a stroke.

TREATMENT-

Minor cases of brain swelling due to causes such as moderate altitude sickness or a slight concussion often resolve within a few days. In most cases, however, more treatment is needed quickly.

The goal is to assure that the brain receives enough blood and oxygen to remain healthy while the swelling is relieved and any underlying causes are treated. This may require a combination of medical and surgical treatments. Prompt treatment usually results in quicker and more complete recovery. Without it, some damage may remain.

Treatment for brain edema may include any combination of the following:

• Oxygen therapy: Providing oxygen through a respirator or other means helps make sure that the blood has enough oxygen in it. The doctor can adjust the respirator to help reduce the amount of swelling.
• IV fluids: Giving fluids and medicine through an IV can keep blood pressure from dropping too low. This helps to make sure that the body — including the brain — is receiving enough blood. However, some fluids can make swelling worse. Doctors attempt to use the right amounts of the right fluids in someone with brain swelling.
• Lowering body temperature (hypothermia): Lowering the temperature of the body and brain helps relieve swelling and allows the brain to heal. Hypothermia as a treatment for brain swelling is not widely used because it is difficult to perform correctly.
• Medication: In some cases of brain edema, your doctor may start a drug to help relieve the swelling. Medication may also be given for other reasons, such as to slow your body’s response to the swelling or to dissolve any clots. The drugs your doctor gives you depend on the cause and symptoms of brain swelling.
• Ventriculostomy: In this procedure, a surgeon cuts a small hole in the skull and inserts a plastic drain tube. Cerebrospinal fluid is drained from inside the brain, helping to relieve the pressure.
• Surgery: Surgery may have one or more of these goals:
  • Removing part of the skull to relieve intracranial pressure; this procedure is called decompressive craniectomy.
  • Removing or repairing the source of the swelling, such as repairing a damaged artery or vein or removing a growth
• Osmotherapy:When your brain swells, it accumulates excess fluid. Osmotherapy is a technique meant to draw water out of the brain. This is done using osmotic agents such as mannitol, or high-salt saline. Osmotic therapy also helps improve blood circulation. This will help reduce swelling and ICP in the skull.

Hyperventilation

Some doctors may perform a controlled hyperventilation to help lower your ICP. Hyperventilation causes you to exhale more than you inhale, lowering the amount of carbon dioxide in your bloodstream. Proper blood flow in your brain is dependent upon carbon dioxide. Controlling this process lowers the blood flow in your brain and reduces ICP.

. Hypothermia

Another treatment method includes inducing hypothermia. Lowering the body temperature decreases metabolism in the brain and can also reduce swelling.

Though there’ve been some success stories with this method, controlled hypothermia is still being researched.

. Ventriculostomy

This is a more invasive procedure that involves draining fluid from the brain. A doctor will make a small incision in the skull and insert a tube as a drain. This method will relieve ICP pressure.

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INTRODUCTION-

Kidney stones, or renal calculi, are solid masses made of crystals. Kidney stones usually originate in your kidneys. However, they can develop anywhere along your urinary tract, which consists of these parts:

• kidneys
• ureters
• bladder
• urethra

Kidney stones are one of the most painful medical conditions. The causes of kidney stones vary according to the type of stone.

Urinary calculi are solid particles in the urinary system. They may cause pain, nausea, vomiting, hematuria, and, possibly, chills and fever due to secondary infection. Diagnosis is based on urinalysis and radiologic imaging, usually noncontrast helical CT. Treatment is with analgesics, antibiotics for infection, medical expulsive therapy, and, sometimes, shock wave lithotripsy or endoscopic procedures.

About 1/1000 adults in the US is hospitalized annually because of urinary calculi, which are also found in about 1% of all autopsies. Up to 12% of men and 5% of women will develop a urinary calculus by age 70. Calculi vary from microscopic crystalline foci to calculi several centimeters in diameter. A large calculus, called a staghorn calculus, can fill an entire renal calyceal system.

Urinary calculi are solid particles in the urinary system. They may cause pain, nausea, vomiting, hematuria, and, possibly, chills and fever due to secondary infection. Diagnosis is based on urinalysis and radiologic imaging, usually noncontrast helical CT. Treatment is with analgesics, antibiotics for infection, medical expulsive therapy, and, sometimes, shock wave lithotripsy or endoscopic procedures.

About 1/1000 adults in the US is hospitalized annually because of urinary calculi, which are also found in about 1% of all autopsies. Up to 12% of men and 5% of women will develop a urinary calculus by age 70. Calculi vary from microscopic crystalline foci to calculi several centimeters in diameter. A large calculus, called a staghorn calculus, can fill an entire renal calyceal system.

Urolithiasis is a common disease, estimated to affect 11% of men and 7% of women in their lifetime. More than 1 million patients with suspected urolithiasis present to an emergency department (ED) each year in the United States.  Ureterolithiasis causes severe unilateral colicky flank pain, and patients usually present within hours of onset. The pain may radiate from the flank anteromedially toward the groin into the genitals and may be accompanied by nausea, vomiting, and hematuria. Passage of a urinary stone is the single most common cause of acute ureteral obstruction and affects as many as 12% of the population. The pain may be some of the most severe pain that humans experience, and complications of stone disease may result in severe infection, renal failure, or, in rare cases, death.

Types of kidney stones-

Not all kidney stones are made up of the same crystals. The different types of kidney stones include:

Calcium

Calcium stones are the most common. They’re often made of calcium oxalate (though they can consist of calcium phosphate or maleate). Eating fewer oxalate-rich foods can reduce your risk of developing this type of stone. High-oxalate foods include:

• potato chips
• peanuts
• chocolate
• beets
• spinach

However, even though some kidney stones are made of calcium, getting enough calcium in your diet can prevent stones from forming.

Uric acid

This type of kidney stone is more common in men than in women. They can occur in people with gout or those going through chemotherapy.

This type of stone develops when urine is too acidic. A diet rich in purines can increase urine’s acidic level. Purine is a colorless substance in animal proteins, such as fish, shellfish, and meats.

Struvite

This type of stone is found mostly in women with urinary tract infections (UTIs). These stones can be large and cause urinary obstruction. They result from a kidney infection. Treating an underlying infection can prevent the development of struvite stones.

Cystine

Cystine stones are rare. They occur in both men and women who have the genetic disorder cystinuria. With this type of stone, cystine — an acid that occurs naturally in the body — leaks from the kidneys into the urine.

CAUSES-

About 85% of calculi in the US are composed of calcium, mainly calcium oxalate (see table Composition of Urinary Calculi); 10% are uric acid; 2% are cystine; most of the remainder are magnesium ammonium phosphate (struvite).

General risk factors include disorders that increase urinary salt concentration, either by increased excretion of calcium or uric acid salts, or by decreased excretion of urinary citrate.For calcium calculi, risk factors vary by population. The main risk factor in the US is hypercalciuria, a hereditary condition present in 50% of men and 75% of women with calcium calculi; thus, patients with a family history of calculi are at increased risk of recurrent calculi. These patients have normal serum calcium, but urinary calcium is elevated > 250 mg/day (> 6.2 mmol/day) in men and > 200 mg/day (> 5.0 mmol/day) in women.

ypocitruria (urinary citrate < 350 mg/day [1820 micromol/day]), present in about 40 to 50% of calcium calculi–formers, promotes calcium calculi formation because citrate normally binds urinary calcium and inhibits the crystallization of calcium salts.

About 5 to 8% of calculi are caused by renal tubular acidosis. About 1 to 2% of patients with calcium calculi have primary hyperparathyroidism. Rare causes of hypercalciuria are sarcoidosis, vitamin D intoxication, hyperthyroidism, multiple myeloma, metastatic cancer, and hyperoxaluria.

Hyperoxaluria (urinary oxalate > 40 mg/day [> 440 micromol/day]) can be primary or caused by excess ingestion of oxalate-containing foods (eg, rhubarb, spinach, cocoa, nuts, pepper, tea) or by excess oxalate absorption due to various enteric diseases (eg, bacterial overgrowth syndromes, chronic pancreatic or biliary disease) or ileojejunal (eg, bariatric) surgery.

Other risk factors include taking high doses of vitamin C (ie, > 2000 mg/day), a calcium-restricted diet (possibly because dietary calcium binds dietary oxalate), and mild hyperuricosuria. Mild hyperuricosuria, defined as urinary uric acid > 800 mg/day (> 5 mmol/day) in men or > 750 mg/day (> 4 mmol/day) in women, is almost always caused by excess intake of purine (in proteins, usually from meat, fish, and poultry); it may cause calcium oxalate calculus formation (hyperuricosuric calcium oxalate nephrolithiasis).

Uric acid calculi most commonly develop as a result of increased urine acidity (urine pH < 5.5), or rarely with severe hyperuricosuria (urinary uric acid > 1500 mg/day [> 9 mmol/day]), which crystallizes undissociated uric acid. Uric acid crystals may comprise the entire calculus or, more commonly, provide a nidus on which calcium or mixed calcium and uric acid calculi can form.

Cystine calculi occur only in the presence of cystinuria.

Magnesium ammonium phosphate calculi (struvite, infection calculi) indicate the presence of a urinary tract infection caused by urea-splitting bacteria (eg, Proteus species, Klebsiella species). The calculi must be treated as infected foreign bodies and removed in their entirety. Unlike other types of calculi, magnesium ammonium phosphate calculi occur 3 times more frequently in women.

Rare causes of urinary calculi include indinavir, melamine, triamterene, and xanthine.

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Pathophysiology-

Urinary calculi may remain within the renal parenchyma or renal collecting system or be passed into the ureter and bladder. During passage, calculi may irritate the ureter and may become lodged, obstructing urine flow and causing hydroureter and sometimes hydronephrosis. Common areas of lodgment include the following:

• Ureteropelvic junction
• Distal ureter (at the level of the iliac vessels)
• Ureterovesical junction

Larger calculi are more likely to become lodged. Typically, a calculus must have a diameter > 5 mm to become lodged. Calculi ≤ 5 mm are likely to pass spontaneously.

Even partial obstruction causes decreased glomerular filtration, which may persist briefly after the calculus has passed. With hydronephrosis and elevated glomerular pressure, renal blood flow declines, further worsening renal function. Generally, however, in the absence of infection, permanent renal dysfunction occurs only after about 28 days of complete obstruction.

Secondary infection can occur with long-standing obstruction, but most patients with calcium-containing calculi do not have infected urine.

SIGN AND SYMPTOM-

Kidney stones are known to cause severe pain. Symptoms of kidney stones may not occur until the stone begins to move down the ureters. This severe pain is called renal colic. You may have pain on one side of your back or abdomen.

In men, pain may radiate to the groin area. The pain of renal colic comes and goes, but can be intense. People with renal colic tend to be restless.

Other symptoms of kidney stones can include:

• blood in the urine (red, pink, or brown urine)
• vomiting
• nausea
• discolored or foul-smelling urine
• chills
• fever
• frequent need to urinate
• urinating small amounts of urine

In the case of a small kidney stone, you may not have any pain or symptoms as the stone passes through your urinary tract.

Large calculi remaining in the renal parenchyma or renal collecting system are often asymptomatic unless they cause obstruction and/or infection. Severe pain, often accompanied by nausea and vomiting, usually occurs when calculi pass into the ureter and cause acute obstruction. Sometimes gross hematuria also occurs.

Pain (renal colic) is of variable intensity but is typically excruciating and intermittent, often occurs cyclically, and lasts 20 to 60 minutes. Nausea and vomiting are common. Pain in the flank or kidney area that radiates across the abdomen suggests upper ureteral or renal pelvic obstruction. Pain that radiates along the course of the ureter into the genital region suggests lower ureteral obstruction. Suprapubic pain along with urinary urgency and frequency suggests a distal ureteral, ureterovesical, or bladder calculus (see Obstructive Uropathy: Symptoms and Signs).

On examination, patients may be in obvious extreme discomfort, often ashen and diaphoretic. Patients with renal colic may be unable to lie still and may pace, writhe, or constantly shift position. The abdomen may be somewhat tender on the affected side as palpation increases pressure in the already-distended kidney (costovertebral angle tenderness), but peritoneal signs (guarding, rebound, rigidity) are lacking.

For some patients, the first symptom is hematuria or either gravel or a calculus in the urine. Other patients may have symptoms of a urinary tract infection, such as fever, dysuria, or cloudy or foul-smelling urine.

RISK FACTORS –

The greatest risk factor for kidney stones is making less than 1 liter of urine per day. This is why kidney stones are common in premature infants who have kidney problems. However, kidney stones are most likely to occur in people between the ages of 20 and 50.

Different factors can increase your risk of developing a stone. In the United States, white people are more likely to have kidney stones than black people.

Sex also plays a role. More men than women develop kidney stones, according to the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK).

A history of kidney stones can increase your risk. So does a family history of kidney stones.

Other risk factors include:

• dehydration
• obesity
• a diet with high levels of protein, salt, or glucose
• hyperparathyroid condition
• gastric bypass surgery
• inflammatory bowel diseases that increase calcium absorption
• taking medications such as triamterene diuretics, antiseizure drugs, and calcium-based antacids

DIAGNOSIS-

• Clinical differential diagnosis
• Urinalysis
• Imaging
• Determination of calculus composition

The symptoms and signs may suggest other diagnoses, such as

• Peritonitis (eg, due to appendicitis, ectopic pregnancy, or pelvic inflammatory disease): Pain is usually constant, and patients lie still because movement worsens pain; patients often also have rebound tenderness or rigidity.
• Cholecystitis: May cause colicky pain, usually in the epigastrium or right upper quadrant, often with Murphy sign.
• Bowel obstruction: May cause colicky abdominal pain and vomiting, but the pain is usually bilateral and not located primarily in the flank or along the ureter.
• Pancreatitis: May cause upper abdominal pain and vomiting, but the pain is usually constant, may be bilateral, and is usually not along the flank or ureter.

With most of these disorders, urinary symptoms are uncommon and other symptoms may suggest which organ system is actually involved (eg, vaginal discharge or bleeding in pelvic disorders among females). Dissecting aortic aneurysm must be considered, particularly in the elderly, because, if a renal artery is affected, it can cause hematuria, pain that radiates along a ureteral distribution, or both. Other considerations in the general evaluation of acute abdominal pain are discussed elsewhere (see Acute Abdominal Pain: Evaluation).Patients suspected of having a calculus causing colic require urinalysis and usually an imaging study. If a calculus is confirmed, evaluation of the underlying disorder, including calculus composition testing, is required.

Urinalysis

Macroscopic or microscopic hematuria is common, but urine may be normal despite multiple calculi. Pyuria with or without bacteria may be present. Pyuria suggests infection, particularly if combined with suggestive clinical findings, such as foul-smelling urine or a fever. A calculus and various crystalline substances may be present in the sediment. If so, further testing is usually necessary because the composition of the calculus and crystals cannot be determined conclusively by microscopy. The only exception is when typical hexagonal crystals of cystine are found in a concentrated, acidified specimen, confirming cystinuria.

Imaging tests

Noncontrast helical CT is the initial imaging study. This study can detect the location of a calculus as well as the degree of obstruction. Moreover, helical CT may also reveal another cause of the pain (eg, aortic aneurysm). For patients who have recurrent calculi, cumulative radiation exposure from multiple CT scans is a concern. However, the routine use of low-dose renal CT can meaningfully reduce cumulative radiation dose with little loss of sensitivity. For patients with typical symptoms, ultrasonography or plain abdominal x-rays can usually confirm presence of a calculus with minimal or no radiation exposure. MRI may not identify calculi.

Although most urinary calculi are demonstrable on plain x-ray, neither their presence nor their absence obviates the need for more definitive imaging, so this study can be avoided except in some patients with suspected recurrent calculi. Both renal ultrasonography and excretory urography (previously called intravenous urography) can identify calculi and hydronephrosis. However, ultrasonography is less sensitive for small or ureteral calculi in patients without hydronephrosis, and excretory urography is time consuming and exposes the patient to the risk of IV contrast agents. These studies are generally used when helical CT is unavailable.

Identifying the cause

The calculus is obtained by straining the urine (or, if necessary, during operative removal) and sent to the laboratory for stone analysis. Some calculi are brought in by patients. Urine specimens that show microscopic crystals are sent for crystallography.

In patients with a single calcium calculus and no additional risk factors for calculi, evaluation to exclude hyperparathyroidism is sufficient. Evaluation entails urinalysis and determination of plasma calcium concentration on 2 separate occasions. Predisposing factors, such as recurrent calculi, a diet high in animal protein, or use of vitamin C or D supplements, should be sought.

Patients with a strong family history of calculi, conditions that might predispose to calculi formation (eg, sarcoidosis, bone metastases, multiple myeloma), or conditions that would make it difficult to treat calculi (eg, solitary kidney, urinary tract anomalies) require evaluation for all possible causative disorders and risk factors. This evaluation should include serum electrolytes, uric acid, and calcium on 2 separate occasions. Follow-up determination of parathyroid hormone levels is done if necessary. Urine tests should include routine urinalysis and 2 separate 24-hour urine collections to determine urine volume, pH, and excretion of calcium, uric acid, citrate, oxalate, sodium, and creatinine. For further information on the medical management of kidney stones, see the guideline of the American Urological Association.

Diagnosis references

• Zilberman DE, Tsivian M, Lipkin ME, et al: Low dose computerized tomography for detection of urolithiasis—its effectiveness in the setting of the urology clinic. J Urol 185(3):910-914, 2011.
• Pearle MS, Goldfarb DS, Assimos DG, et al: Medical management of kidney stones—AUA guideline. J Urology 92(2):316-24, 2014.

PREVENTION-

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Proper hydration is a key preventive measure. drinking enough water to pass about 2.6 quarts of urine each day. Increasing the amount of urine you pass helps flush the kidneys.

You can substitute ginger ale, lemon-lime soda, and fruit juice for water to help you increase your fluid intake. If the stones are related to low citrate levels, citrate juices could help prevent the formation of stones.

Eating oxalate-rich foods in moderation and reducing your intake of salt and animal proteins can also lower your risk of kidney stones.

Your doctor may prescribe medications to help prevent the formation of calcium and uric acid stones. If you’ve had a kidney stone or you’re at risk for a kidney stone, speak with your doctor and discuss the best methods of prevention.

In a patient who has passed a first calcium calculus, the likelihood of forming a 2nd calculus is about 15% at 1 year, 40% at 5 years, and 80% at 10 years. Drinking large amounts of fluids—8 to 10 ten-ounce (300-milliliter) glasses a day—is recommended for prevention of all stones. Recovery and analysis of the calculus, measurement of calculus-forming substances in the urine, and the clinical history are needed to plan other prophylactic measures.

In < 3% of patients, no metabolic abnormality is found. These patients seemingly cannot tolerate normal amounts of calculus-forming salts in their urine without crystallization. Thiazide diuretics, potassium citrate, and increased fluid intake may reduce their calculus production rate.

For hypercalciuria, patients may receive thiazide diuretics (eg, chlorthalidone 25 mg orally once a day or indapamide 1.25 mg orally once a day) to lower urine calcium excretion and thus prevent urinary supersaturation with calcium oxalate. Patients are encouraged to increase their fluid intake to ≥ 3 L/day. A diet that is low in sodium and high in potassium is recommended. Even with a high potassium intake, supplementation with potassium citrate is recommended to prevent hypokalemia. Restriction of dietary animal protein is also recommended.

For patients with hypocitruria, potassium citrate (20 mEq [20 mmol/L] orally twice a day) enhances citrate excretion. A normal calcium intake (eg, 1000 mg or about 2 to 3 dairy servings per day) is recommended, and calcium restriction is avoided. Oral orthophosphate has not been thoroughly studied. Alternative alkaline agents (eg, sodium or potassium bicarbonate) can be used to enhance citrate excretion.

Hyperoxaluria prevention varies. Patients with small-bowel disease can be treated with a combination of high fluid intake, calcium loading (usually in the form of calcium citrate 400 mg orally twice a day with meals), cholestyramine, and a low-oxalate, low-fat diet. Hyperoxaluria may respond to pyridoxine 100 to 200 mg orally once a day, possibly by increasing transaminase activity, because this activity is responsible for the conversion of glyoxylate, the immediate oxalate precursor, to glycine.

In hyperuricosuria, intake of animal protein should be reduced. If the diet cannot be changed, allopurinol 300 mg each morning lowers uric acid production. For uric acid calculi, the urine pH must be increased to between 6 and 6.5 by giving an oral alkalinizing drug that contains potassium (eg, potassium citrate 20 mEq [20 mmol/L] twice a day) along with increased fluid intake.

Infection with urea-splitting bacteria requires culture-specific antibiotics and complete removal of all calculi. If eradication of infection is impossible, long-term suppressive therapy (eg, with nitrofurantoin) may be necessary. In addition, acetohydroxamic acid can be used to reduce the recurrence of struvite calculi.

To prevent recurrent cystine calculi, urinary cystine levels must be reduced to < 250 mg cystine/L of urine. Any combination of increasing urine volume along with reducing cystine excretion (eg, with alpha-mercaptopropionylglycine [tiopronin] or penicillamine) should reduce the urinary cystine concentration.

TREATMENT-

• Analgesia
• Facilitate calculus passage, eg, with alpha-receptor blockers such as tamsulosin (described as medical expulsive therapy)
• For persistent or infection-causing calculi, complete removal using primarily endoscopic techniques

Analgesia

Renal colic may be relieved with opioids, such as morphine and, for a rapid onset, fentanyl. Ketorolac 30 mg IV is rapidly effective and nonsedating. Vomiting usually resolves as pain decreases, but persistent vomiting can be treated with an antiemetic (eg, ondansetron 10 mg IV).

Medical expulsive therapy

Although increasing fluids (either oral or IV) has traditionally been recommended, increased fluid administration has not been proven to speed the passage of calculi. Patients with calculi < 1 cm in diameter who have no infection or obstruction, whose pain is controlled with analgesics, and who can tolerate liquids can be treated at home with analgesics and alpha-receptor blockers (eg, tamsulosin 0.4 mg orally once a day) to facilitate calculus passage. Calculi that have not passed within 6 to 8 weeks typically require removal. In patients with infection and obstruction, initial treatment is relief of obstruction with a ureteral stent and treatment of the infection followed by removal of calculi as soon as possible.

Pain relief may require narcotic medications. The presence of infection requires treatment with antibiotics. Other medications include:

• allopurinol (Zyloprim) for uric acid stones
• thiazide diuretics to prevent calcium stones from forming
• sodium bicarbonate or sodium citrate to make the urine less acidic
• phosphorus solutions to prevent calcium stones from forming
• ibuprofen (Advil) for pain
• acetaminophen (Tylenol) for pain
• naproxen sodium (Aleve) for pain

Calculus removal

The technique used for removal depends on the location and size of the calculus. Techniques include shock wave lithotripsy and, to ensure complete removal or for larger calculi, endoscopic techniques. Endoscopic techniques may involve rigid or flexible ureteroscopes (endoscopes) and may involve direct-vision removal (basketing), fragmentation with some sort of lithotripsy device (eg, pneumatic, ultrasonic, laser), or both.

For symptomatic calculi < 1 cm in diameter in the renal collecting system or proximal ureter, shock wave lithotripsy is a reasonable first option for therapy.

For larger calculi or if shock wave lithotripsy is unsuccessful, ureteroscopy (done in a retrograde fashion) with holmium laser lithotripsy is usually used. Sometimes removal is possible using an endoscope inserted anterograde through the kidney. For renal stones > 2 cm, percutaneous nephrolithotomy, with insertion of a nephroscope directly into the kidney, is the treatment of choice.

For midureteral calculi, ureteroscopy with holmium laser lithotripsy is usually the treatment of choice. Shock wave lithotripsy is an alternative.

For distal ureteral calculi, endoscopic techniques (ureteroscopy), such as direct removal and use of intracorporeal lithotripsy (eg, holmium laser, pneumatic), are considered by many to be the procedures of choice. Shock wave lithotripsy can also be used.

Calculus dissolution

Uric acid calculi in the upper or lower urinary tract occasionally may be dissolved by prolonged alkalinization of the urine with potassium citrate 20 mEq (20 mmol/L) orally 2 to 3 times a day, but chemical dissolution of calcium calculi is not possible and of cystine calculi is difficult.

Lithotripsy

Extracorporeal shock wave lithotripsy uses sound waves to break up large stones so they can more easily pass down the ureters into your bladder. This procedure can be uncomfortable and may require light anesthesia. It can cause bruising on the abdomen and back and bleeding around the kidney and nearby organs.

Ureteroscopy

When a stone is stuck in the ureter or bladder, your doctor may use an instrument called a ureteroscope to remove it.

A small wire with a camera attached is inserted into the urethra and passed into the bladder. The doctor then uses a small cage to snag the stone and remove it. The stone is then sent to the laboratory for analysis.

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INTRODUCTION-

An aneurysm occurs when an artery’s wall weakens and causes an abnormally large bulge. This bulge can rupture and cause internal bleeding. Although an aneurysm can occur in any part of your body, they’re most common in the:

• brain
• aorta
• legs
• spleen

About 13,000 deathsTrusted Source occur each year in the United States from aortic aneurysms.

brain aneurysm (AN-yoo-riz-um) is a bulge or ballooning in a blood vessel in the brain. It often looks like a berry hanging on a stem.

A brain aneurysm can leak or rupture, causing bleeding into the brain (hemorrhagic stroke). Most often a ruptured brain aneurysm occurs in the space between the brain and the thin tissues covering the brain. This type of hemorrhagic stroke is called a subarachnoid hemorrhage.

A ruptured aneurysm quickly becomes life-threatening and requires prompt medical treatment.

Most brain aneurysms, however, don’t rupture, create health problems or cause symptoms. Such aneurysms are often detected during tests for other conditions.

Treatment for an unruptured brain aneurysm may be appropriate in some cases and may prevent a rupture in the future. Talk with your caregiver to ensure you understand the best options for your specific needs.

CAUSES-

Although the exact cause of an aneurysm is unclear, certain factors contribute to the condition.

For example, damaged tissue in the arteries can play a role. The arteries can be harmed by blockages, such as fatty deposits. These deposits can trigger the heart to pump harder than necessary to push blood past the fatty buildup. This stress can damage the arteries because of the increased pressure.

Atherosclerotic disease

Atherosclerotic disease can also lead to an aneurysm. People with atherosclerotic disease have a form of plaque buildup in their arteries. Plaque is a hard substance that damages the arteries and prevents blood from flowing freely.

High blood pressure

High blood pressure may also cause an aneurysm. The force of your blood as it travels through your blood vessels is measured by how much pressure it places on your artery walls. If the pressure increases above a normal rate, it may enlarge or weaken the blood vessels.

Blood pressure for an adult is considered normal at or below 120/80 mm Hg, or millimeters of mercury.

A significantly higher blood pressure can increase the risk for heart, blood vessel, and circulation problems. Higher-than-normal blood pressure doesn’t necessarily put you at risk for an aneurysm.

TYPES-

An aneurysm may occur anywhere in your body, but these are the most common locations of aneurysms:

Aorta

The aorta is the largest blood vessel in the body. It begins at the left ventricle of the heart and travels down the abdomen where it splits off into both legs. The aorta is a common site for arterial aneurysms.

• Aneurysms in the chest cavity are called thoracic aortic aneurysms.
• Abdominal aortic aneurysms are the most common type. In rare cases, both the chest and abdomen can be affected by arterial damage.

Brain

Aneurysms in the brain can be any size. These often form in the blood vessels that lie deep within the brain. They also may not present any symptoms or signs. You may not even know you have an aneurysm. Brain aneurysms of this type may cause bleeding in as many as 3 percent of people.

Other areas

You can also have an aneurysm in the artery behind your knee, in your spleen, or in your intestines.

SYMPTOM-

Symptoms of an aneurysm vary with each type and location. It’s important to know that aneurysms that occur in the body or brain generally don’t present signs or symptoms until they rupture.

Aneurysms that occur near the surface of the body may show signs of swelling and pain. A large mass may also develop. The symptoms of ruptured aneurysms anywhere in the body can include:

• bleeding
• increased heart rate
• pain
• feeling dizzy or lightheaded

Serious complications from aneurysms can cause death if you don’t get emergency care.

Ruptured aneurysm

A sudden, severe headache is the key symptom of a ruptured aneurysm. This headache is often described as the “worst headache” ever experienced.

Common signs and symptoms of a ruptured aneurysm include:

• Sudden, extremely severe headache
• Nausea and vomiting
• Stiff neck
• Blurred or double vision
• Sensitivity to light
• Seizure
• A drooping eyelid
• Loss of consciousness
• Confusion

‘Leaking’ aneurysm

In some cases, an aneurysm may leak a slight amount of blood. This leaking (sentinel bleed) may cause only a:

• Sudden, extremely severe headache

A more severe rupture often follows leaking.

‘Leaking’ aneurysm

In some cases, an aneurysm may leak a slight amount of blood. This leaking (sentinel bleed) may cause only a:

• Sudden, extremely severe headache

A more severe rupture often follows leaking.

Unruptured aneurysm

An unruptured brain aneurysm may produce no symptoms, particularly if it’s small. However, a larger unruptured aneurysm may press on brain tissues and nerves, possibly causing:

• Pain above and behind one eye
• A dilated pupil
• Change in vision or double vision
• Numbness of one side of the face

When to see a doctor

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Seek immediate medical attention if you develop a:

• Sudden, extremely severe headache

If you’re with someone who complains of a sudden, severe headache or who loses consciousness or has a seizure, call 911 or your local emergency number.

Brain aneurysms develop as a result of thinning artery walls. Aneurysms often form at forks or branches in arteries because those sections of the vessel are weaker.

Although aneurysms can appear anywhere in the brain, they are most common in arteries at the base of the brain.

DIAGNOSIS-

The diagnostic tools used to find arterial damage often depend on the location of the problem. Your doctor may refer you to a specialist like a cardiothoracic or vascular surgeon.

CT scans and ultrasound methods are common tools used to diagnose or find blood vessel irregularities. CT scans use X-rays to examine the inside of your body. This allows your doctor to see the condition of the blood vessels, as well as any blockages, bulges, and weak spots that may be inside the blood vessels.

RISK FACTOR-

A number of factors can contribute to weakness in an artery wall and increase the risk of a brain aneurysm or aneurysm rupture. Brain aneurysms are more common in adults than in children and more common in women than in men.

Some of these risk factors develop over time; others are present at birth.

Risk factors that develop over time

These include:

• Older age
• Cigarette smoking
• High blood pressure (hypertension)
• Drug abuse, particularly the use of cocaine
• Heavy alcohol consumption

Some types of aneurysms may occur after a head injury (dissecting aneurysm) or from certain blood infections (mycotic aneurysm).

Risk factors present at birth

Selected conditions that date to birth can be associated with an elevated risk of developing a brain aneurysm. These include:

• Inherited connective tissue disorders, such as Ehlers-Danlos syndrome, that weaken blood vessels
• Polycystic kidney disease, an inherited disorder that results in fluid-filled sacs in the kidneys and usually increases blood pressure
• Abnormally narrow aorta (coarctation of the aorta), the large blood vessel that delivers oxygen-rich blood from the heart to the body
• Cerebral arteriovenous malformation (brain AVM), an abnormal connection between arteries and veins in the brain that interrupts the normal flow of blood between them
• Family history of brain aneurysm, particularly a first-degree relative, such as a parent, brother, sister, or child.

COMPLICATION-

When a brain aneurysm ruptures, the bleeding usually lasts only a few seconds. The blood can cause direct damage to surrounding cells, and the bleeding can damage or kill other cells. It also increases pressure inside the skull.

If the pressure becomes too elevated, the blood and oxygen supply to the brain may be disrupted to the point that loss of consciousness or even death may occur.

Complications that can develop after the rupture of an aneurysm include:

• Re-bleeding. An aneurysm that has ruptured or leaked is at risk of bleeding again. Re-bleeding can cause further damage to brain cells.
• Vasospasm. After a brain aneurysm ruptures, blood vessels in your brain may narrow erratically (vasospasm). This condition can limit blood flow to brain cells (ischemic stroke) and cause additional cell damage and loss.
• Hydrocephalus. When an aneurysm rupture results in bleeding in the space between the brain and surrounding tissue (subarachnoid hemorrhage) — most often the case — the blood can block circulation of the fluid surrounding the brain and spinal cord (cerebrospinal fluid). This condition can result in an excess of cerebrospinal fluid that increases pressure on the brain and can damage tissues (hydrocephalus).
• Hyponatremia. Subarachnoid hemorrhage from a ruptured brain aneurysm can disrupt the balance of sodium in the blood. This may occur from damage to the hypothalamus, an area near the base of the brain. A drop in blood-sodium levels (hyponatremia) can lead to swelling of brain cells and permanent damage.

PREVENTION-

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Eating a healthy diet containing plenty of fruits, whole grains, and vegetables may help prevent an aneurysm from forming. Meat and poultry low in saturated fat and cholesterol are also good options for protein. Low-fat dairy products are also beneficial.

Regular exercise, especially cardio, can encourage healthy blood circulation and blood flow through the heart, arteries, and other blood vessels.

If you smoke tobacco products, now is the time to quit. Eliminating tobacco can decrease your risk for an aneurysm.

You should also see your doctor for annual checkups.

TREATMENT-

Treatment typically depends on the location and type of aneurysm.

For example, a weak area of a vessel in your chest and abdomen may require a type of surgery called an endovascular stent graft. This minimally invasive procedure may be chosen over traditional open surgery because it involves repairing and reinforcing damaged blood vessels. The procedure also reduces the chance of infection, scarring, and other problems.

Other treatments can include medications that treat high blood pressure and high cholesterol. Certain types of beta-blockers may also be prescribed to lower blood pressure. Lowering your blood pressure may keep your aneurysm from rupturing.

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INTRODUCTION-

A thrombus is a blood clot in the circulatory system. It attaches to the site at which it formed and remains there, hindering blood flow.

Doctors describe the development of a thrombus as thrombosis.

A thrombus is most likely to occur in people who are immobile and in those with a genetic predisposition to blood clotting.

A thrombus can also form after damage occurs in an artery, vein, or surrounding tissue.In this article, we look at blood clotting and the different types of thrombi. We also look at the symptoms, diagnosis, and treatment of a thrombus.

TYPES-

Thrombosis occurs when blood clots block your blood vessels. There are 2 main types of thrombosis:

• Venous thrombosis is when the blood clot blocks a vein. Veins carry blood from the body back into the heart.
• Arterial thrombosis is when the blood clot blocks an artery. Arteries carry oxygen-rich blood away from the heart to the body.

A blood clot is usually a normal physical response to injury.

It quickly forms a plug that can reduce or prevent bleeding. However, a thrombus can cause severe health problems, as it interrupts the function of a blood vessel.

A section of a blood clot that breaks free from the thrombus and circulates in the bloodstream is called an embolus.

An embolus moves through the vascular system until it lodges in a different part of the body.

An embolus is a dangerous and potentially fatal complication of thrombosis. It is especially dangerous if it reaches the heart, lungs, or brain (embolism).

Doctors categorize thrombi based on the type of blood vessel in which they develop:

When a thrombus forms in an artery, such as in the heart or brain, it is called an arterial thrombosis.

When a thrombus occurs in a vein, it is called a venous thrombosis. When this happens in the deep veins of the leg, it is called deep vein thrombosis (DVT).

CAUSES-

Clotting occurs due to a series of chemical reactions between blood cells known as platelets and proteins called clotting factors.

When a person is in good health, the body regulates the clotting process according to its needs.

However, a clot can form more easily when a person:

• uses tobacco
• has high cholesterol
• has obesity or is overweight
• has cancer
• has diabetes
• is stressed
• has an inactive lifestyle

Venous thrombosismay be caused by:

• Disease or injury to the leg veins
• Not being able to move around (immobility) for any reason
• A broken bone (fracture)
• Certain medicines
• Obesity
• Inherited disorders, or a greater likelihood of having a certain disorder based on your genes
• Autoimmune disorders that make it more likely your blood will clot
• Medicines that increase your risk of clotting (such as certain birth control medicines)

Arterial thrombosismay be caused by a hardening of the arteries, called arteriosclerosis. This happens when fatty or calcium deposits cause artery walls to thicken. This can lead to a buildup of fatty material (called plaque) in the artery walls. This plaque can suddenly burst (rupture), followed by a blood clot.

Arterial thrombosis can occur in the arteries that supply blood to the heart muscle (coronary arteries). This can lead to a heart attack. When arterial thrombosis occurs in a blood vessel in the brain, it can lead to a stroke.

Some of these factors also increase the risk of atherosclerosis, a condition wherein fatty plaque deposits line the blood vessels and clog them.

Atherosclerosis makes blood clots more likely to block the arteries and the veins.

SYMPTOM-

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Each person’s symptoms may vary. Symptoms may include:

• Pain in one leg (usually the calf or inner thigh)
• Swelling in the leg or arm
• Chest pain
• Numbness or weakness on one side of the body
• Sudden change in your mental state

The symptoms of thrombosis may look like other blood disorders or health problems. Always see your healthcare provider for a diagnosis.

Deep vein thrombosis signs and symptoms can include:

Swelling in the affected leg. Rarely, there’s swelling in both legs.

• Pain in your leg. The pain often starts in your calf and can feel like cramping or soreness.
• Red or discolored skin on the leg.
• A feeling of warmth in the affected leg.

Deep vein thrombosis can occur without noticeable symptoms.

When to see a doctor

If you develop signs or symptoms of deep vein thrombosis, contact your doctor.

If you develop signs or symptoms of a pulmonary embolism — a life-threatening complication of deep vein thrombosis — seek immediate medical attention.

The warning signs and symptoms of a pulmonary embolism include:

• Sudden shortness of breath
• Chest pain or discomfort that worsens when you take a deep breath or when you cough
• Feeling lightheaded or dizzy, or fainting
• Rapid pulse
• Coughing up blood

Symptoms of arterial thrombosis

A thrombus in an artery can result in:

• unstable angina, which is a type of chest pain
• heart attack
• ischemic stroke
• peripheral arterial limb ischemia, a condition that significantly reduces blood flow to the limbs

These conditions all require prompt medical attention.

People should seek emergency treatment if they experience any of the following symptoms:

• chest pain
• shortness of breath
• drooping on the lower half of the face
• a sudden loss of strength in one arm or leg
• a limb that has become cold, pale, and painful

Diagnosis

Doctors use several different methods to diagnose the presence of a thrombus. For example, they may use:

• Duplex ultrasound: This is the most common test for diagnosing DVT. A duplex ultrasound uses sound waves to create images of the blood flowing through the arteries and veins.
• A D-dimer test: This test measures the levels of a substance in the blood that results from the breakdown of blood clots. High levels of this substance may indicate the presence of DVT or another type of blood clot. However, the test is not definitive. If the result is normal and few risk factors are present, a person does not have a high risk of DVT.
• Venography: For venography, a doctor will inject a dye into a vein in the affected leg. This dye makes the vein visible on some types of X-ray, such as a fluoroscopy. If the scan shows a slower-than-usual blood flow through the vein, a thrombus may be present.
• MRI and CT scans: These scans create detailed images of organs, tissues, and blood vessels.
• A VQ scan: This is a nuclear imaging study. It uses a radioactive substance called a radiotracer to reveal, on a scan, the flow of air and blood within the lungs.

A doctor may request blood tests to check for a genetic blood clotting disorder. This may be necessary in cases of repeated unexplained blood clots.Thrombi in the liver, kidney, or brain may develop due to an inherited clotting disorder.

RISK FACTOR-

Many of the risk factors for venous and arterial thrombosis are the same.

Risk factors for venous thrombosis may include:

• A family history of a blood clot in a vein deep in the body, called a deep vein thrombosis (DVT)
• A history of DVT
• Hormone therapy or birth control pills
• Pregnancy
• Injury to a vein, such as from surgery, a broken bone, or other trauma
• Lack of movement, such as after surgery or on a long trip
• Inherited blood clotting disorders
• A central venous catheter
• Older age
• Smoking
• Being overweight or obese
• Some health conditions, such as cancer, heart disease, lung disease, or Crohn’s disease

Risk factors for arterial thrombosis may include:

• Smoking
• Diabetes
• High blood pressure
• High cholesterol
• Lack of activity and obesity
• Poor diet
• Family history of arterial thrombosis 
• Lack of movement, such as after surgery or on a long trip
• Older age

Many factors can increase your risk of developing deep vein thrombosis (DVT). The more you have, the greater your risk of DVT. Risk factors include:

• Inheriting a blood-clotting disorder. Some people inherit a disorder that makes their blood clot more easily. This condition on its own might not cause blood clots unless combined with one or more other risk factors.
• Prolonged bed rest, such as during a long hospital stay, or paralysis. When your legs remain still for long periods, your calf muscles don’t contract to help blood circulate, which can increase the risk of blood clots.
• Injury or surgery. Injury to your veins or surgery can increase the risk of blood clots.
• Pregnancy. Pregnancy increases the pressure in the veins in your pelvis and legs. Women with an inherited clotting disorder are especially at risk. The risk of blood clots from pregnancy can continue for up to six weeks after you have your baby.
• Birth control pills (oral contraceptives) or hormone replacement therapy. Both can increase your blood’s ability to clot.
• Being overweight or obese. Being overweight increases the pressure in the veins in your pelvis and legs.
• Smoking. Smoking affects blood clotting and circulation, which can increase your risk of DVT.
• Cancer. Some forms of cancer increase substances in your blood that cause your blood to clot. Some forms of cancer treatment also increase the risk of blood clots.
• Heart failure. This increases your risk of DVT and pulmonary embolism. Because people with heart failure have limited heart and lung function, the symptoms caused by even a small pulmonary embolism are more noticeable.
• Inflammatory bowel disease. Bowel diseases, such as Crohn’s disease or ulcerative colitis, increase the risk of DVT.
• A personal or family history of deep vein thrombosis or pulmonary embolism. If you or someone in your family has had one or both of these, you might be at greater risk of developing a DVT.
• Age. Being older than 60 increases your risk of DVT, though it can occur at any age.
• Sitting for long periods of time, such as when driving or flying. When your legs remain still for hours, your calf muscles don’t contract, which normally helps blood circulate. Blood clots can form in the calves of your legs if your calf muscles don’t move for long periods.

COMPLICATION-

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Thrombosis can block the blood flow in both veins and arteries. Complications depend on where the thrombosis is located. The most serious problems include stroke, heart attack, and serious breathing problems.

A serious complication associated with deep vein thrombosis is pulmonary embolism.

Pulmonary embolism

A pulmonary embolism occurs when a blood vessel in your lung becomes blocked by a blood clot (thrombus) that travels to your lung from another part of your body, usually your leg.

A pulmonary embolism can be life-threatening. It’s important to watch for signs and symptoms of a pulmonary embolism and seek medical attention if they occur. Signs and symptoms of a pulmonary embolism include:

• Sudden shortness of breath
• Chest pain or discomfort that worsens when you take a deep breath or when you cough
• Feeling lightheaded or dizzy, or fainting
• Rapid pulse
• Coughing up blood

Postphlebitic syndrome

A common complication that can occur after deep vein thrombosis is known as postphlebitic syndrome, also called postthrombotic syndrome. Damage to your veins from the blood clot reduces blood flow in the affected areas, which can cause:

• Persistent swelling of your legs (edema)
• Leg pain
• Skin discoloration
• Skin sores

PREVENTION-

You can reduce your risk of thrombosis by:

• Being active
• Getting back to activity as soon as possible after surgery
• Exercising your legs during long trips
• Quitting smoking
• Losing weight
• Managing other health problems such as diabetes, high blood pressure, and high cholesterol

Measures to prevent deep vein thrombosis include:

• Avoid sitting still. If you have had surgery or have been on bed rest for other reasons, try to get moving as soon as possible. If you’re sitting for a while, don’t cross your legs, which can hamper blood flow. If you’re traveling a long distance by car, stop every hour or so and walk around. If you’re on a plane, stand or walk occasionally. If you can’t do that, exercise your lower legs. Try raising and lowering your heels while keeping your toes on the floor, then raising your toes with your heels are on the floor.
• Make lifestyle changes. Lose weight and quit smoking.
• Exercise. Regular exercise lowers your risk of blood clots, which is especially important for people who sit a lot or travel frequently.

It is not always possible to prevent a thrombus. However, people can take steps to reduce their risk.

For example, a person can:

• avoid or quit tobacco smoking
• prevent excessive weight gain or lose weight to avoid obesity
• adopt a healthful diet
• exercise regularly

It is particularly important for a person to move around as much as possible after a surgical procedure or during long distance travel.

Those with a higher risk of developing a blood clot may also require anticoagulant therapy alongside medications to reduce blood pressure and blood cholesterol levels.

TREATMENT-

The aim of treating a thrombus is to achieve the following quickly and effectively:

• gain control over the symptoms
• restore the blood flow
• reduce and remove the thrombus

Doctors typically recommend the following treatments to deal with the effects of thrombi:

Surgery

Surgery for the effects of thrombosis will always be a medical emergency.

The procedure can involve directly accessing and unblocking an affected artery. In other cases, the surgeon will divert blood flow or completely bypass the blocked artery.

Inferior vena cava filters

Inferior vena cava (IVC) filters are small mesh devices that a surgeon can put in the inferior vena cava (a large vein), usually under local anesthetic.

The IVC filter traps fragments of the blood clot and prevents them from reaching the heart and lungs.

An IVC filter can be permanent, and doctors typically combine this treatment with anticoagulation medication therapy where possible. However, a surgeon may remove the IVC filter if the person’s risk of a blood clot declines.

Anticoagulants

Anticoagulants, or blood thinners, have a misleading name; they do not give the blood a thinner consistency.

Instead, they reduce the risk of a clot forming, which can reduce the size of a thrombus.

When taking anticoagulant medications, a person should visit a specialized anticoagulant management service instead of a primary care physician.

If anticoagulants are not effective, or if a person does not tolerate them well, a doctor will consider other treatment options.

Compression stockings

Doctors may recommend that people wear compression stockings while taking anticoagulant therapy for DVT.

The stockings help prevent calf pain and swelling, as well as reduce the risk of complications.

A person should wear compression stockings for as long as their doctor recommends.

Raising the affected leg

As well as wearing compression stockings, people should try to keep the affected leg elevated above hip level during the night.

This can relieve pressure in the veins, improve blood circulation, and help prevent complications.

Exercise

Once a doctor has prescribed compression stockings, they will usually recommend more frequent walking to stimulate blood circulation.

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INTRODUCTION-

Most of the nerves in your body are covered with a protective layer called myelin. It’s a lot like the insulation on electric wires. It helps messages from your brain move quickly and smoothly through your body, the way electricity flows from a power source.

Demyelinating disorders are any conditions that damage myelin. When this happens, scar tissue forms in its place. Brain signals can’t move across scar tissue as quickly, so your nerves don’t work as well as they should.

The peripheral nerves consist of bundles of long neuronal axons as they exit the central nervous system (CNS). Some peripheral nerves are wrapped in a myelin sheath generated by Schwann cells, whereas others are unmyelinated. Peripheral nerves serve different motor, sensory, and autonomic functions. The term peripheral neuropathy is usually used to describe symmetric and universal damage to adjacent nerves. The damage and clinical manifestations are usually located distally with a proximal progression. Several disorders can damage peripheral nerves and cause peripheral neuropathy; it is important to differentiate actual neuropathy from other disorders that can have a similar clinical presentation.

Peripheral neuropathy has a variety of systemic, metabolic, and toxic causes. The most common treatable causes include diabetes mellitus, hypothyroidism, and nutritional deficiencies. The diagnosis requires careful clinical assessment, judicious laboratory testing, and electrodiagnostic studies or nerve biopsy if the diagnosis remains unclear. A systematic approach begins with localization of the lesion to the peripheral nerves, identification of the underlying etiology, and exclusion of potentially treatable causes. Initial blood tests should include a complete blood count, comprehensive metabolic profile, and measurement of erythrocyte sedimentation rate and fasting blood glucose, vitamin B₁₂, and thyroid-stimulating hormone levels; specialized tests should be ordered if clinically indicated. Lumbar puncture and cerebrospinal fluid analysis may be helpful in the diagnosis of Guillain-Barré syndrome and chronic inflammatory demyelinating neuropathy. Electrodiagnostic studies, including nerve conduction studies and electromyography, can help in the differentiation of axonal versus demyelinating or mixed neuropathy. Treatment should address the underlying disease process, correct any nutritional deficiencies, and provide symptomatic treatment.

Symptoms and Signs-

A host of symptoms and signs that reflect sensory, motor, and autonomic nerve fiber dysfunction are typical of peripheral neuropathies, and some combinations of symptoms and signs may be recognized as specific syndromes of peripheral nerve disease. Sensory symptoms include sensory loss, often described by patients as a sense of numbness or a “Novocain-like” feeling. In most generalized polyneuropathies, these symptoms begin in the most distal extent of the longest sensory fibers (i.e., those that subserve sensation in the toes and feet). The pathologic changes in most of these polyneuropathies are those of a distal-to-proximal axonal degeneration that have been referred to as distal axonopathies or dying-back neuropathies. Similar symptoms may be seen in hereditary or acquired demyelinating polyneuropathies.

Sensory Symptoms

Typically, all sensory modalities are affected to some extent, including light touch, pain, thermal sensation, vibratory sense, and joint position sense. As the disease progresses, sensory loss ascends the lower extremities, typically in a symmetrical fashion. When the sensory loss is at or above the level of the knee, the axons supplying the distal fingertips begin to be involved, and the length-dependent process then begins in the upper extremities. In addition to sensory loss, patients often complain of paresthesias and dysesthesias, often characterized by a sense of numbness, tingling, prickling, and pins-and-needles sensations. They might also complain of intense bandlike sensations and feelings of pressure.

The sensory examination often discloses a distal-to-proximal loss of the various sensory modalities. In certain polyneuropathies, pain predominates in the clinical picture, and the sensory examination tends to disclose deficits predominantly of pain and thermal sensation, conforming to an SFN. On occasion, when significant proprioceptive deafferentation occurs, patients are found to have altered joint position sense that can manifest as an ataxia or tremor of the affected limbs and an imbalance of gait and station.

Pain is a serious symptom for many patients. It may be described as a dull aching sensation, an intense burning sensation or, occasionally, as intermittent lancinating pulses of pain. On occasion, patients notice that their skin is hypersensitive to tactile stimulation such as from the touch of bed sheets or clothing or from standing on their feet. Some patients note an exaggerated painful sensation resulting from any stimulus to the affected area, a form of pain termed allodynia.

Weakness

Impairment of motor function typically produces weakness in a distal-to-proximal gradient consistent with a length-dependent axonal degeneration. As with sensory loss, weakness begins in the toes, and as the polyneuropathy progresses, it ascends up the distal lower extremities to the level of the knees, at which time motor involvement in the hands may be observed. Similar patterns of weakness may be seen in demyelinating polyneuropathies. However, in the acquired segmental demyelinating polyneuropathies such as CIDP and related disorders, proximal muscle weakness resulting from root involvement may be observed outside the proximal-to-distal gradient of the dying-back mechanism. This pattern of involvement is termed a polyradiculoneuropathy.

Axonal degenerative polyneuropathies tend to produce weakness along with muscle atrophy, but atrophy is much less conspicuous in segmental demyelinating polyneuropathies because in these disorders the axon remains in continuity with the muscle, preventing denervation atrophy. The most common symptom in polyneuropathy is weakness in dorsiflexion of the feet at the ankles. This can result in a partial or complete foot drop that typically causes the feet to slap while walking and predisposes the patient to stumble and fall when the toes catch on an uneven surface.

Tendon reflexes are usually depressed or absent in a distal-to-proximal pattern of involvement, with the lower extremities affected more than the upper extremities. An exception to this is in SFN, in which the large-caliber sensory afferent fibers from muscle spindles are relatively preserved and the tendon reflexes might remain intact.

Autonomic Symptoms

In some polyneuropathies, typically in SFN, autonomic fibers are also affected. In these disorders, a variety of autonomic symptoms may be present, although certainly the most dramatic and incapacitating is orthostatic hypotension, which causes postural light- headedness, syncope, or both. However, orthostatic hypotension typically occurs only with advanced autonomic involvement.

Earlier in the course of autonomic neuropathy, patients might notice reduced or absent sweating (i.e., anhidrosis) often in a distal-to-proximal gradient. Some patients complain of excessive sweating confined to the head and neck region. This is most often secondary to anhidrosis in the limbs and thorax and reflects compensatory hyperhidrosis in the restricted areas that maintain normal sweating.

Other autonomic symptoms include dryness of the eyes and mouth and gastrointestinal dysmotility, often manifested by alternating constipation and diarrhea or by early satiety from gastroparesis. In addition, patients may have urinary bladder dysfunction caused by an atonic bladder, which results in overflow incontinence. In men, erectile dysfunction can represent an early autonomic symptom, reflecting parasympathetic autonomic nervous system involvement.

Other Symptoms and Signs

Various limb deformities and trophic changes may be observed in chronic polyneuropathies. Pes cavus, characterized by high arches and hammer toes and the clawfoot deformity, are typical foot deformities in hereditary polyneuropathies with childhood onset. These deformities are a result of progressive weakness and atrophy of intrinsic foot muscles. A similar claw-like deformity may be observed in the hand.

Autonomic involvement of a limb may, at times, cause the affected area to appear warm, red, and swollen and at other times pale and cold because of abnormal regulation of small vessels as a result of autonomic denervation. Various trophic changes can occur including tight, shiny skin.

In patients who have had severe sensory loss in the limbs, the affected areas may be subject to incidental traumas, including burns, pressure sores, and other injuries that are not perceived by the patient. In these patients, repeated injuries and traumas can result in chronic infections, sometimes leading to osteomyelitis.

In peripheral nerve disorders that are focal and asymmetrical, sensory and motor—and occasionally autonomic—symptoms and signs may conform to a specific peripheral nerve distribution. For example, in carpal tunnel syndrome, patients might complain of intermittent numbness and tingling in the median nerve distribution in the hand or, as the entrapment progresses, atrophy and weakness of the thenar muscle group. In the mononeuritis multiplex syndrome, multiple individual peripheral nerves may be affected, and the sensory, motor, and autonomic symptoms and signs will be distributed in a multifocal pattern conforming to numerous individual peripheral nerve lesions. On occasion, some peripheral nerve disorders cause generalized sensory and motor fiber involvement with asymmetrical and focal features.

Prevalence and Risk Factors-

Peripheral nerve disorders are relatively common conditions that affect 2.4% of the population. However, the prevalence increases to 8.0% with advancing age.

The most common generalized polyneuropathy is diabetic sensorimotor polyneuropathy, which may be present in as many as 66% of type 1 diabetes patients and in nearly 59% of type 2 diabetes patients.Even higher prevalence rates have been reported depending on the criteria used to diagnose polyneuropathy. Considering that the prevalence rate of diabetes is approximately 1.3%, this common complication of diabetes could affect nearly 1% of the general population.

The most common genetic sensorimotor polyneuropathy is Charcot-Marie-Tooth disease type 1a, which has a prevalence of approximately 30 per 100,000 population. Carpal tunnel syndrome, caused by chronic entrapment of the median nerve in the carpal tunnel, is the most common mononeuropathy, with a prevalence estimated to be between 3% and 5% of adults.

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Diagnosis

Diagnosis begins by recognizing typical symptoms of peripheral nerve disease and identifying the pattern of peripheral nerve involvement. For example, if the symptoms are highly restricted and focal, they might conform to the distribution of an individual peripheral nerve or, possibly, to an individual root. More-diffuse involvement of an entire limb might be caused by involvement of the brachial or lumbosacral plexus. Alternatively, if generalized symptoms are distributed in an asymmetrical and focal fashion, they may be consistent with a mononeuritis multiplex picture or possibly a polyradiculoneuropathy or polyradiculopathy syndrome. Most often, peripheral neuropathies produce symptoms that are generalized and relatively symmetrical, conforming to a distal-to-proximal gradient typical of a distal axonopathy.

History and Physical Examination

As soon as their distribution is recognized, the symptoms should be analyzed to determine which fiber types appear to be involved (i.e., sensory, motor, autonomic). In addition, the temporal profile of the disorder (i.e., chronic, subacute, acute) is noted. The neurologic examination is then helpful in confirming signs of sensory, motor, or autonomic dysfunction and in documenting the pattern and fiber type involved. These clinical features, which can be derived solely from the history and physical examination, are valuable for characterizing the nature of the peripheral nerve syndrome, which is essential in constructing a differential diagnosis.

Electrodiagnostic Studies

Another important component to the evaluation of peripheral nerve disease is electrodiagnostic studies, primarily nerve conduction studies and the needle electrode examination. Electrodiagnostic testing can document the presence of peripheral nerve disease, define the distribution and pattern of various sensory and motor fibers, and characterize the underlying pathologic processes (i.e., wallerian degeneration, axonal degeneration, segmental demyelination, or some mixture of these pathologic reactions). Characterizing the electrodiagnostic features, particularly whether the process is axonal or demyelinating, adds additional information.⁴

Medical Studies

Other special studies include lumbar puncture for cerebrospinal fluid analysis, which may be useful in diagnosing inflammatory or infectious causes of polyneuropathy, in evaluating acquired demyelinating polyneuropathies such as those in GBS and CIDP, and in a variety of immune-mediated polyneuropathies.

Nerve biopsy, typically sural nerve biopsy, is most often recommended in patients with asymmetrical or focal polyneuropathies in whom a diagnosis of vasculitis is being considered. In addition, biopsies may be used to assist in the diagnosis of some inflammatory, infectious, and metabolic polyneuropathies. Nerve biopsy can help to establish the pathologic basis of the polyneuropathy when electrodiagnostic studies cannot conclusively distinguish an axonal from an acquired segmental demyelinating disorder.

Special autonomic studies, particularly those that measure cardiovascular autonomic reflexes (including heart rate response to deep breathing, heart rate and blood pressure responses to the Valsalva maneuver, and heart rate and blood pressure responses to head-up-tilt) may also be valuable in documenting autonomic cardiovascular involvement. Various tests of sudomotor function including the sympathetic skin response, quantitative sudomotor axon reflex test, and thermoregulatory sweat testing can provide valuable information regarding the extent and distribution of sudomotor impairment in polyneuropathy.

Skin biopsy to measure epidermal nerve fiber density is also a helpful test for the diagnosis of SFN. Quantitative sensory testing is a technique that allows precise measurement of sensory perception thresholds of various fiber types, which can also be helpful in assessing peripheral neuropathy, especially SFN, in which the electrodiagnostic studies are often normal.

Laboratory Studies

By recognizing the peripheral nerve syndrome and appreciating the potential differential diagnosis, one may systematically perform appropriate medical tests to explore the various possible causes. The most common peripheral nerve syndrome is the generalized sensorimotor polyneuropathy with electrodiagnostic features of a distal axonopathy. For this disorder, it is usually appropriate to pursue a history of toxin exposure (see Tables 2 and 3) and alcoholism with nutritional deficiency. It is also reasonable to perform routine laboratory screening studies including a complete blood cell count; erythrocyte sedimentation rate; a blood chemistry panel encompassing hepatic function, renal function, and electrolytes; thyroid function studies; and vitamin B₁₂ level.

It is important to screen patients for diabetes mellitus. In the past, a fasting blood sugar or hemoglobin A_1c, or both, was often performed, but recent reports suggest that impaired glucose tolerance detected on a glucose tolerance test might provide more meaningful information regarding diabetes as a potential cause for polyneuropathy.⁵

Screening the serum and urine with protein electrophoresis with immunofixation is also important in assessing patients with generalized polyneuropathy. In one series, the only laboratory tests that were helpful in establishing a precise cause for the polyneuropathy were vitamin B₁₂, serum protein electrophoresis with immunofixation, and serum glucose.Additional laboratory and radiographic studies may be considered pending the specific clinical features, and may include chest radiograph, skeletal bone survey, antinuclear antibodies, rheumatoid factor, and angiotensin-converting enzyme level.

In patients with an aggressive, evolving polyneuropathy or a specific paraneoplastic syndrome, additional testing for an occult malignancy is often performed, usually in conjunction with autoantibodies, especially anti-Hu. A variety of autoantibodies have been associated with different polyneuropathy syndromes. The most useful of these include anti-GM₁ antibodies in the setting of MMNCB, anti-Hu antibodies in the context of a sensory neuronopathy, and anti-myelin-associated glycoprotein antibodies in acquired demyelinating polyneuropathy with predominately sensory features and with a distal pattern of involvement. Most of the other antibodies are much less specific, and their roles in the mechanism of the polyneuropathies are less certain. Thus, the precise value of performing panels of antibody tests is unclear at this time.

Lumbar puncture is often reserved for patients with possible immune-mediated polyneuropathies, particularly those with demyelinating features on electrodiagnostic testing. However, CSF studies are also often assessed in cryptogenic axonal degeneration polyneuropathies and in patients with possible infectious or inflammatory disorders.

Epidemiology

One study estimated that the prevalence of peripheral neuropathy in the family medicine setting is 8 percent in persons 55 years and older. The prevalence in the general population may be as high as 2.4 percent. A community-based study estimated the prevalence of peripheral neuropathy in patients with type 2 diabetes mellitus to be 26.4 percent.

TREATMENT-

Medical Treatment

Specific therapies for polyneuropathy are based on the precise etiologic diagnosis. In disorders attributed to underlying medical conditions, management is focused on the medical disorder. For example, optimizing glycemic control in diabetic polyneuropathy often stabilizes or improves the polyneuropathy.

In patients with idiopathic immune-mediated polyneuropathies, including GBS, CIDP, and MMNCB, specific immune-modulating therapies are often recommended.^8,11 For GBS, intravenous gamma globulin (IVIg), typically administered at a dosage of 400 mg/kg daily for 5 consecutive days, is initiated early in the patient’s course. Alternatively, plasmapheresis may also be instituted as initial therapy.

Treatment of CIDP may begin with corticosteroid therapy. However, chronic IVIg or plasmapheresis, or both, are usually effective and obviate the need for long-term steroid therapy. Alternative therapies including azathioprine, cyclophosphamide, cyclosporine, mycophenolate mofetil, methotrexate, and rituximab have also been used in patients who have not responded to initial standard therapies.

Toxic polyneuropathies are managed by discontinuing the offending drug or removing the industrial toxin from the patient’s environment.

Management of hereditary polyneuropathies includes education of the affected family members regarding the nature and genetic features of the disorder and judicious screening of family members at risk.

Supportive Therapy

For all patients, and particularly for those without a specific or treatable cause, therapy focuses on supportive measures. This may include the use of various physical therapy and occupational therapy modalities including bracing and aids to ambulation. An ankle-foot orthosis may be effective in improving ambulation in a patient with foot drop. In patients with severe sensory loss in the feet and lower extremities, careful daily foot inspection for signs of trauma and infection are essential to prevent serious infections and other complications.

Pain Management

In patients who have associated pain, particularly patients with SFN, specific neuropathic pain management is instituted. Neuropathic pain typically does not respond to simple analgesics, and its potential chronicity precludes narcotic therapy as a first choice. Typically, patients with SFN and other painful polyneuropathies respond to drugs known to be effective for neuropathic pain, including tricyclic antidepressants and a variety of antiepileptic drugs and membrane stabilizers.

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INTRODUCTION-

Brain and spinal cord lesions have an increasing social and economic importance. Accidental trauma of various kinds is the main cause of mortality of children and young adults in developed countries. Only cardiac disease and cancer surpass the number of death caused by accidents and, examining the number of potential work years lost, CNS lesions surpass all other problems. Most brain and spinal cord injuries cause chronic incapacity and frequently occur to individuals under 45 years of age. Edema and other acute events can be efficiently treated and CNS lesions may not be mortal, but are incurable.

Traumatic Brain Injury (TBI) is a disruption in the normal function of the brain that can be caused by a blow, bump or jolt to the head, the head suddenly and violently hitting an object or when an object pierces the skull and enters brain tissue. Observing one of the following clinical signs constitutes alteration in the normal brain function:

• Loss of or decreased consciousness
• Loss of memory for events before or after the event (amnesia)
• Focal neurological deficits such as muscle weakness, loss of vision, change in speech
• Alteration in mental state such as disorientation, slow thinking or difficulty concentrating

Symptoms of a TBI can be mild, moderate, or severe, depending on the extent of damage to the brain. Mild cases may result in a brief change in mental state or consciousness. Severe cases may result in extended periods of unconsciousness, coma, or even death.

he final outcome of CNS injury depend on the area damaged and the extent of the lesion, but the best present therapies can offer is relief of the symptoms and rehabilitation. This review examines the present state of functional repair of experimental central nervous system trauma.

TRAUMA-

Cellular infiltrates in the CSF of victims of CNS trauma are indistinguishable from the cells seen in subarachnoid hemorrhage and destructive lesions of other etiologies. Thus, red blood cells and macrophages containing hemosiderin or myelin debris are the most common manifestations of trauma in CSF. Patients with sinus and basilar skull fractures with tears in the meninges are at risk for developing leakage of sinus contents into the SAS. The CSF in this setting contains a marked acute inflammatory reaction. Bacteria and other elements, such as fragments of Candida and ciliated respiratory epithelial cells from the sinus lining, may also be seen.

Key features of trauma•

Red blood cells; and•

Macrophages containing hemosiderin or myelin debris.

The Problem

Traumatic brain injury (TBI) remains a major health problem with serious socio-economic consequences. Although its incidence is decreasing in most western countries according to some estimates, severe TBI will become the third most common cause of death and disability globally by the year 2020.

In 1996, 3740 deaths from serious injuries were recorded in the United Kingdom. The death rate for all ages from a head injury in the United Kingdom is 9 deaths per 100,000 population per year, or 1% of all deaths, or 15-20% of deaths of persons aged 5-35 years

CAUSES-

Brain trauma can be caused by a direct impact or by acceleration alone. In addition to the damage caused at the moment of injury, brain trauma causes secondary injury, a variety of events that take place in the minutes and days following the injury. These processes, which include alterations in cerebral blood flow and the pressure within the skull, contribute substantially to the damage from the initial injury.

TYPES-

Brain injuries can be classified into mild, moderate, and severe categories. The Glasgow Coma Scale (GCS), the most commonly used system for classifying TBI severity, grades a person’s level of consciousness on a scale of 3–15 based on verbal, motor, and eye-opening reactions to stimuli. It is generally agreed that a TBI with a GCS of 13 or above is mild, 9–12 is moderate, and 8 or below is severe.

TBIs can cause “mass lesions,” w an area of localized injury such as hematomas and contusions that increase pressure within the brain. Summarized below are different types of sequelae deveoped from TBIs:

Hematoma: A hematoma is a blood clot within the brain or on its surface. Hematomas may occur anywhere within the brain. An epidural hematoma is a collection of blood between the dura mater (the protective covering of the brain) and the inside of the skull. A subdural hematoma is a collection of blood between the dura mater and the arachnoid layer, which sits directly on the surface of the brain.

Contusion: A cerebral contusion is bruising of brain tissue. When examined under a microscope, cerebral contusions are comparable to bruises in other parts of the body. They consist of areas of injured or swollen brain mixed with blood that has leaked from arteries, veins, or capillaries. Most commonly, contusions are at the base of the front parts of the brain, but may occur anywhere.

Intracerebral Hemorrhage: An intracerebral hemorrhage (ICH) describes bleeding within the brain tissue, may be related to other brain injuries, especially contusions. The size and location of the hemorrhage helps determine whether it can be removed surgically.

Subarachnoid Hemorrhage: Subarachnoid hemorrhage (SAH) is caused by bleeding into the subarachnoid space. It appears as diffuse blood spread thinly over the surface of the brain and commonly after TBI. Most cases of SAH associated with head trauma are mild. Hydrocephalus may result from severe traumatic SAH.

Diffuse Injuries: TBIs can produce microscopic changes that do not appear on CT scans and are scattered throughout the brain. This category of injuries, called diffuse brain injury, may occur with or without an associated mass lesion.

Diffuse Axonal Injury: Axonal injury refers to impaired function and gradual loss of axons.These long extensions of nerve cells enable them to communicate with each other. If enough axons are harmed in this way, the ability of nerve cells to communicate with each other and to integrate their function may be lost or greatly impaired, possibly leaving a patient with severe disabilities.

Ischemia: Another type of diffuse injury is ischemia or insufficient blood supply to certain parts of the brain. A decrease in blood supply to very low levels may occur commonly in a significant number of TBI patients. This is crucial since a brain that has just undergone a traumatic injury is especially sensitive to slight reductions in blood flow. Changes in blood pressure during the first few days after head injury can also have an adverse effect.

Skull Fractures: Linear skull fractures or simple breaks or “cracks” in the skull may accompany TBIs.

Possible forces, strong enough to cause a skull fracture may damage the underlying brain. Skull fractures may be alarming, if found on a patient evaluation. Fractures at the base of the skull are problematic since they can cause injury to nerves, arteries, or other structures. If the fracture extends into the sinuses, a leakage of cerebrospinal fluid (CSF) from the nose or ears may occur. Depressed skull fractures, in which part of the bone presses on or into the brain, can also occur.

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SYMPTOM-

Symptoms vary greatly depending on the severity of the head injury. They may include any of the following:

• Vomiting
• Lethargy
• Headache
• Confusion
• Paralysis
• Coma
• Loss of consciousness
• Dilated pupils
• Vision changes (blurred vision or seeing double, unable to tolerate bright light, loss of eye movement, blindness)
• Cerebrospinal fluid (CSF) (clear or blood-tinged) appear from the ears or nose
• Dizziness and balance concerns
• Breathing problems
• Slow pulse
• Slow breathing ratewith an increase in blood pressure
• Ringing in the ears or changes in hearing
• Cognitive difficulties
• Inappropriate emotional responses
• Speech difficulties (slurred speech, inability to understand and/or articulate words)
• Difficulty swallowing
• Body numbness or tingling
• Droopy eyelid or facial weakness
• Loss of bowel control or bladder control

If a TBI is suspected, call 911 immediately or take the person to an emergency room.

Side Effects and Complications

Subdural hematoma is a possible result of traumatic head injury: In this image, the single arrow marks spread of the subdural haematoma and the double arrow marks the midline shift.

TBI can cause a host of physical, cognitive, social, emotional, and behavioral effects, and the outcome can range from complete recovery to permanent disability or death. The 20^th century saw critical developments in diagnosis and treatment that decreased death rates and improved outcome. Some of the current imaging techniques used for diagnosis and treatment include CT scans (computed tomography) and MRIs (magnetic resonance imaging). Depending on the injury, treatment required may be minimal or may include interventions such as medications, emergency surgery or surgery years later. Physical therapy, speech therapy, recreation therapy, and occupational therapy may be employed for rehabilitation.

Complications are distinct medical problems that may arise as a result of the TBI. TBI can cause prolonged or permanent effects on consciousness, such as coma, brain death, persistent vegetative state (in which patients are unable to achieve a state of alertness to interact with their surroundings), and minimally conscious state. Lying still for long periods can cause complications including pressure sores, pneumonia or other infections, progressive multiple organ failure, and deep venous thrombosis, which can cause pulmonary embolism. Complications involving the blood vessels include vasospasm, in which vessels constrict and restrict blood flow, the formation of aneurysms, in which the side of a vessel weakens and balloons out, and stroke. Movement disorders that may develop after TBI include tremor, ataxia (uncoordinated muscle movements), myoclonus (shock-like contractions of muscles), and loss of movement range and control (in particular with a loss of movement repertoire). The risk of post-traumatic seizures increases with severity of trauma and is particularly elevated with certain types of brain trauma such as cerebral contusions or hematomas.

TESTING AND DIAGNOSIS-

Anyone with signs of moderate or severe TBI should receive medical attention as soon as possible. Because we cannot do much to reverse the initial brain damage caused by trauma, medical providers try to stabilize an individual with TBI and focus on preventing further injury.

First, the cardiac and pulmonary function is assessed. Next, a quick examination of the entire body is performed, followed by a complete neurological examination. The neurological examination includes an assessment utilizing the Glasgow Coma Scale (GCS). In addition to the GCS, also tested is the ability of the pupils to become smaller in bright light. In patients with large mass lesions or with high intracranial pressure (ICP), one or both pupils may be very wide or “blown.” The presence of a wide or dilated pupil on only one side suggests a large mass lesion may be present. Brainstem reflexes including gag and corneal (blink) may also be tested.

Radiological Tests

A computed tomography scan (CT or CAT scan) is the gold standard for the radiological assessment of a TBI patient. A CT scan is easy to perform and an excellent test for detecting the presence of blood and fractures, the most crucial lesions to identify in medical trauma cases. Plain x-rays of the skull are recommended by some as a way to evaluate patients with only mild neurological dysfunction. However, most centers in the U.S. have readily available CT scanning, a more accurate test, rendering the routine use of skull x-rays for TBI patients to decline.

Magnetic resonance imaging (MRI) is not commonly used for acute head injury since it takes longer to perform a MRI than a CT. Because it is difficult to transport an acutely-injured patient from the emergency room to a MRI scanner, the use of MRI is impractical. However, once a patient is stabilized, MRI may demonstrate the existence of lesions that were not detected on the CT scan. This information is generally more useful for determining prognosis than for influencing treatment.

TREATMENT-

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Surgery–

Many patients with moderate or severe head injuries head directly from the emergency room to the operating room. In many cases, surgery is performed to remove a large hematoma or contusion that is significantly compressing the brain or raising the pressure within the skull. After surgery, these patients are under observation in the intensive care unit (ICU).

Other head-injured patients may not head to the operating room immediately, instead are taken from the emergency room to the ICU. Since contusions or hematomas may enlarge over the first hours or days after head injury, immediate surgery is not recommended on these patients until several days after their injury. Delayed hematomas may be discovered when a patient’s neurological exam worsens or when their ICP increases. On other occasions, a routine follow-up CT scanto determine whether a small lesion has changed in size indicates that the hematoma or contusion has enlarged significantly. In these cases, the safest approach is to remove the lesion before it enlarges and causes neurological damage.

During surgery, the hair over the affected part of the head is usually shaved. After the scalp incision, the removed bone is extracted in a single piece or flap, then replaced after surgery unless contaminated. The dura mater is carefully cut to reveal the underlying brain. After any hematoma or contusion is removed, the neurosurgeon ensures the area is not bleeding. He or she then closes the dura, replaces the bone and closes the scalp. If the brain is very swollen, some neurosurgeons may decide not to replace the bone until the swelling decreases, which may take up to several weeks. The neurosurgeon may elect to place an ICP monitor or other types of monitors if these were not already in place. The patient is returned to the ICU for observation and additional care.

Non-Surgical Treatments

At present, medication administered to prevent nerve damage or promote nerve healing after TBI not available. The primary goal in the ICU is to prevent any secondary injury to the brain. The “primary insult” refers to the initial trauma to the brain, whereas the “secondary insult” is any subsequent development that may contribute to neurological injury. For example, an injured brain is especially sensitive and vulnerable to decreases in blood pressure otherwise well tolerated. One way to avoid secondary insults is to attempt normal or slightly elevated blood pressure levels. Likewise, increases in ICP, decreases in blood oxygenation, increases in body temperature, increases in blood glucose and many other disturbances can potentially worsen neurological damage. The major role of ICU management is the prevention of secondary insults in head-injured patients.

Various monitoring devices may assist health care personnel in caring for the patient. Placement of an ICP monitor into the brain can help detect excessive swelling. One commonly used type of ICP monitor is a ventriculostomy, a narrow, flexible, hollow catheter that is passed into the ventricles, or fluid spaces in the center of the brain, to monitor ICP and drain CSF if ICP increases. Another commonly used type of intracranial pressure monitoring device involves placement of a small fiberoptic catheter directly into the brain tissue. Additional catheters may be added to measure brain temperature and brain tissue oxygenation. Placement of an oxygen sensor into the jugular vein can detect how much oxygen the brain is using. This may be related to the degree of brain damage. Many other monitoring techniques currently under investigation to determine whether they can help improve outcome after head injury or provide additional information about caring for TBI patients.

Rehabilitation

Once head-injured patients leave the acute-care hospital, some benefit from a rehabilitation program. Prime candidates for rehabilitation are patients with less severe initial injuries or those that started to show significant improvement.

In some cases, transfer to a rehabilitation hospital or to the rehabilitation service of a large hospital may expedite further recovery. For more severely injured patients or those with slow recovery, constant vigilance is required to prevent the gradual onset of problems with joint mobility, skin integrity, respiratory status, infection and many other physiological functions. Patients with moderate or mild injuries, or severely injured patients who have improved sufficiently, are likely candidates for outpatient therapy.

Most head-injury rehabilitation centers emphasize compensatory strategies to help patients learn to reach the maximum level of function allowed by their impairments. The concept of cognitive retraining, a controversial concept, which presumes that at least some of the brain’s cognitive capacity can be restored by constant repetition of certain simple tasks, is also emphasized at many centers. Head injury rehabilitation centers work with patients’ families to educate them about realistic expectations and best help their injured family member.

General Head Injury Prevention Tips

• Wear a seatbelt every time you drive or ride in a motor vehicle.
• Never drive while under the influence of drugs, alcohol or ride as a passenger with anyone who is under the influence.
• Keep firearms unloaded in a locked cabinet or safe, and store ammunition in a separate, secure location.
• Remove hazards in the home that may contribute to falls. Secure rugs and loose electrical cords, put away toys, use safety gates and install window guards. Install grab bars and handrails if you are frail or elderly.

Sports and Recreation Head Injury Prevention Tips

• For specific sports, 100 percent of the time, buy and use helmets or protective headgear approved by the American Society for Testing and Materials (ASTM).
• Supervise younger children at all times.
• Do not allow younger children to use sporting equipment or play sports unsuitable for their age.
• Avoid the use of playgrounds with hard surfaces.
• Follow all rules and warning signs at water parks, swimming pools and public beaches.
• Do not dive in water less than 12 feet deep or in above-ground pools. Check the depth – and check for debris in the water before diving.
• Wear appropriate clothing for the sport.
• Do not wear any clothing that can interfere with your vision.
• Do not participate in sports when you are ill or very tired.
• Obey all traffic signals, and be aware of drivers when cycling or skateboarding.
• Avoid uneven or unpaved surfaces when cycling, skateboarding or in-line skating.
• Perform regular safety checks of sports fields, playgrounds and equipment.
• Discard and replace damaged sporting equipment or protective gear
• Never slide head-first when stealing a base.

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