Diagnostic Approach of Insomnia

Diagnostic Approach of Insomnia

1. How long have you had problems with insomnia?

   Why: to determine if acute or chronic. Transient insomnia can last up to 3-4 weeks and after that it is considered to be chronic.

2. Is the sleep disturbance problem with sleep onset (initial insomnia), sleep maintenance (middle insomnia) or premature awakening (late insomnia)?
3. What is the sleeping environment?

   Why: Common problems with the sleeping environment that may contribute to insomnia and sleep disturbance include noise, extreme temperatures, poorly ventilated room, hot bedroom, cold bedroom, mattress that is too soft or hard, too much light in bedroom.

4. Do you take day time naps?

   Why: may cause or prolong the problem of insomnia.

5. What is the age of the person with insomnia?

   Why: a reduction in sleep requirements often accompanies aging. If the sleep disturbance is in a child or infant must consider hunger, colic, indigestion, dirty diaper, too hot, too cold, teething.

6. Are there simple reasons for sleep disturbance?

   Why: e.g. overeating before bedtime, sugar snack before bedtime, environment change (in an unfamiliar hotel or hospital bed), sleep schedule change, jet lag, shift work, mental stimulation before bedtime, sex at bedtime (some people become stimulated after sex), lack of exercise, partner who has restless legs syndrome or who snores loudly.

7. What are your stressors at the moment?

   Why: questions specifically about relationship, family, children, social support, occupation, general physical health and financial stresses. Stressors are a common cause of insomnia such as a change of occupation, loss of a loved one, illness, anxiety over a deadline or examination.

8. Previous or current use of sedatives or hypnotics?

   Why: The regular use of sedatives or hypnotics will interfere with sleep patterns and lead to chronic insomnia. Often the dosage of these medications will have been increased in the past so as to maintain hypnotic effectiveness after tolerance begins to develop. In cases of withdrawal, individuals may sleep only 1-4 hours each night ("rebound insomnia") for several weeks and will also experience an increase in anxious dr and nightmares and awakenings through the night.

9. Past medical history?

   Why: many medical problems may increase the risk of insomnia such as hyperthyroidism, kidney disease, Parkinson's disease, asthma, congestive cardiac failure, emphysema, chronic bronchitis, Addison's disease, Cushing's disease.

10. Past psychiatric history?

    Why: certain mental illnesses are well known to cause insomnia such as depression, anxiety, schizophrenia, mania.

11. Medications?

    Why: Some medications may cause insomnia including thyroid hormones, certain weight loss drugs, phenylpropanolamine (PPA), nasal decongestants, diuretics (due to night urination), high-potency vitamins, certain antidepressants (e.g. SSRIs and also MAOs). Withdrawal of some medications may also cause insomnia such as severe rebound insomnia with benzodiazepine sleeping pills.

12. Cigarette smoking?

    Why: may cause insomnia especially at bedtime. The use of nicotine patches for smoking cessation may cause vivid dreams and disturbed sleep in some people.

13. Alcohol history?

    Why: excessive alcohol before bedtime may cause insomnia. Typically alcohol causes increased drowsiness and reduced time to fall to sleep but even moderate amounts of alcohol can increase awakenings after sleep onset by interfering with the ability of the brain to maintain sleep.

14. Caffeine intake?

    Why: including coffee, tea, cola, chocolate (especially before bedtime but even in the afternoon in some people) may cause insomnia. It causes an increased time to fall to sleep, more frequent arousals during sleep, and a reduction in total sleep time for up to 8-14 hours after caffeine ingestion.

15. Illicit drug use?

    Why: e.g. amphetamine and cocaine usage may cause insomnia.

Sometimes, other symptoms may be present and may help your doctor analyse your condition. These may include:

1. Night urination?

   Why: causes of night time urination such as cystitis, prostatitis, benign enlargement of the prostate, prostate cancer, diuretic usage and diabetes may effectively cause insomnia due to the practical need to urinate.

2. Pain or physical discomfort?

   Why: any disease that causes any discomfort may interfere with sleep such as chronic back pain, arthritis pain, peptic ulcer pain, angina chest pain, skin ulcer pain, ear ache, tooth ache, anal itch, leg cramps.

3. Shortness of breath at night?

   Why: any disease that causes shortness of breath especially at night may interfere with sleep such as congestive heart failure, asthma, emphysema.

4. Symptoms of hyperthyroidism?

   Why: e.g. loose bowel motions, intolerance to heat, sweating of hands, muscle weakness, increased appetite, weight loss, heart palpitations, emotional disturbance, sleep disturbance.

5. Symptoms of menopause?

   Why: e.g. hot flushes, night sweats, heart palpitations, lightheadedness, dry vaginal, dry skin, headaches, disturbed sleep due to night sweats and hot flushes.

6. Symptoms of depression?

   Why: e.g. depressed mood, crying spells, anhedonia (loss of interest or pleasure), increase or decrease in appetite (usually decreased), weight loss or gain, insomnia or increased sleeping, fatigue, loss of energy, feelings of worthlessness, feelings of excessive guilt, poor concentration, difficulty making decisions, low libido, thoughts of death or suicide attempt. The great majority of individuals who experience major depression will suffer form insomnia, usually early morning wakening (usually around 3am) with difficulty returning to sleep.

7. Symptoms of anxiety?

   Why: e.g. nervousness, shakiness, tremor, restlessness, irritability, insomnia, poor concentration, heart palpitations, racing heart, sweating, dizziness, diarrhea, lump in throat and frequency of urination. Difficulty with getting to sleep (both at the beginning of the night and following night time awakenings) is a common feature of generalized anxiety disorder, due to increased autonomic arousal and worry.

8. Symptoms of Manic-depression?

   Why: e.g. episodes of depression (often psychotic in intensity) and at other times episodes of psychotic excitement (mania or hypomania). Symptoms of psychotic excitement may include elevation of mood, increased activity, insomnia, decreased need for sleep, grandiose ideas, irritability, disinhibition (which affects social, sexual and financial behavior), rapid speech and racing thought, delusions (persecutory or grandiose) and sometimes hallucinations.

9. Symptoms of restless leg syndrome?

   Why: e.g. irresistible urge to move their legs when awake and inactive, especially when lying in bed just prior to sleep. This interferes with the ability to fall asleep. People experience a creeping, crawling sensation deep in their calves that is only relieved by movement, particularly walking.

10. Symptoms of obstructive sleep apnea?

    Why: e.g. loud snoring, disturbed nocturnal sleep, daytime sleepiness, unrefreshed sleep, restless sleep, morning headache, nocturnal choking, reduced libido.

11. Symptoms of narcolepsy?

    Why: e.g. excessive daytime sleepiness wit involuntary daytime sleep episodes, disturbed nocturnal sleep and cataplexy (sudden weakness or loss of muscle tome, often elicited by emotion).

12. Symptoms of Parkinson's disease?

    Why: e.g. coarse hand tremor most marked at rest, rigidity of limbs, slowness in initiating and executing movements and speech, expressionless mask-like face and dementia. Sufferers of Parkinson's disease frequently complain of difficulty getting to sleep and increased awake time during the night.

Pneumothorax

Pneumothorax

What is a pneumothorax?

A pneumothorax is a collection of free air in the chest outside the lung that causes the lung to collapse.

Types of pneumothorax

A spontaneous pneumothorax, also referred to as a primary pneumothorax, occurs in the absence of a traumatic injury to the chest or a known lung disease. A secondary (also termed complicated) pneumothorax occurs as a result of an underlying condition.

Causes

• Spontaneously (more commonly in tall slim young males and in Marfan syndrome)
• Following a penetrating chest wound
• Following barotrauma to the lungs^[2][3]

It may also be due to:

• Chronic lung pathologies including emphysema, asthma
• Acute infections
• Chronic infections, such as tuberculosis
• Lung damage caused by cystic fibrosis
• Lung Cancer
• Rare diseases that are unique to women such as Catamenial pneumothorax (due to endometriosis in the chest cavity) and lymphangioleiomyomatosis (LAM).

Symptoms

Almost everyone who has a collapsed lung has the following symptoms:

• Sharp chest pain, made worse by a deep breath or a cough
• Shortness of breath

A larger pneumothorax will cause more severe symptoms, including:

• Chest tightness
• Easy fatigue
• Rapid heart rate
• Bluish color of the skin caused by lack of oxygen

Note: Symptoms may begin during rest or sleep.

Other symptoms that can occur with a collapsed lung include:

• Nasal flaring
• Low blood pressure (hypotension)

Investigations

• Chest x-ray to tell whether there is air outside the lung
• Arterial blood gases

Treatment

A small pneumothorax may go away on its own. You may only need oxygen and rest. The health care provider may use a needle to pull the extra air out from around the lung so it can expand more fully. You may be allowed to go home if you live near the hospital.

If you have a large pneumothorax, a chest tube will be placed between the ribs into the space around the lungs to help drain the air and allows the lung to re-expand.

The chest tube can be left in place for several days. You must stay in the hospital while the chest tube is in place.

Some patients with a collapsed lung need extra oxygen, which helps the air around the lung be reabsorbed more quickly.

Lung surgery may be needed to treat your pneumothorax or to prevent future episodes. The area where the leak occurred may be repaired. Sometimes, a special chemical is placed into the area of the collapsed lung. This chemical causes a scar to form.

Expectations (prognosis)

If you have a collapsed lung, you are more likely to have another one in the future if you:

• Are tall and thin

• Continue to smoke

• Have had two collapsed lungs in the past

How well a person does after having a collapsed lung depends on what caused it.

Complications

• Another collapsed lung in the future

• Shock

Pleural effusion

What is a pleural effusion?

A pleural effusion is an excess accumulation of fluid in the pleural space around the lungs. The pleura are thin membranes that enclose the lungs and line the inside of the chest cavity. The 'pleural space' describes the small space between the inner and outer layers of pleura, which normally contains a small volume of lubricating pleural fluid to allow the lungs to expand without friction. This fluid is constantly being formed through leakage of fluid from nearby capillaries and then re-absorbed by the body's lymphatic system. With a pleural effusion, some imbalance between production and reabsorption of pleural fluid leads to excess fluid building up in the pleural space.

There are two major types of pleural effusion:

• Transudative effusions, where the excess pleural fluid is low in protein; and
• Exudative effusions, where the excess pleural fluid is high in protein

Types of fluids

Four types of fluids can accumulate in the pleural space:

• Serous fluid (hydrothorax)
• Blood ([haemothorax])
• Chyle (chylothorax)
• Pus (pyothorax or empyema)

Causes of Pleural Effusions

Anything that causes an imbalance between production and reabsorption of pleural fluid can lead to development of a pleural effusion. Transudative pleural effusions (those low in protein) usually form as a result of excess capillary fluid leakage into the pleural space. Common causes of transudative effusions include:

• Congestive heart failure;
• Nephrotic syndrome;
• Cirrhosis of the liver;
• Pulmonary embolism; and
• Hypothyroidism.

Exudative effusions, which are high in protein, are often more serious than transudative effusions. They are formed as a result of inflammation of the pleura, which might happen for example in lung disease. Common causes of exudative effusions include:

• Pneumonia;
• Lung cancer, or other cancers;
• Connective tissue diseases, including rheumatoid arthritis and systemic lupus erythematosus;
• Pulmonary embolism;
• Asbestosis;
• Tuberculosis; and
• Radiotherapy.

Clinical Diagniosis;

Physical findings are variable and depend on the volume of the pleural effusion. Generally, there are no physical findings for effusions smaller than 300 mL. With effusions larger than 300 mL, findings may include the following:

• Dullness to percussion
• Decreased tactile fremitus
• Asymmetric chest expansion, with diminished or delayed expansion on the side of the effusion: Dullness to percussion, decreased tactile fremitus, and asymmetric chest expansion are the most reliable physical findings of pleural effusion.
• Diminished or inaudible breath sounds
• Egophony ("e" to "a" changes) at the most superior aspect of the pleural effusion
• Pleural friction rub
• Other findings that provide clues to the etiology of the effusion include the following:
  • Peripheral edema, distended neck veins, and S ₃ gallop, suggestive of congestive heart failure
  • Edema may also be a manifestation of nephrotic syndrome; pericardial disease; or, combined with yellow nails, the yellow nail syndrome.
  • Cutaneous changes with ascites, suggestive of liver disease
  • Evidence of malignancy such as lymphadenopathy or palpable mass

Investigations

During a physical examination, the doctor will listen to the sound of your breathing with a stethoscope and may tap on your chest to listen for dullness.

The following tests may help to confirm a diagnosis:

• Chest x-ray
• Pleural fluid analysis (examining the fluid under a microscope to look for bacteria, amount of protein, and presence of cancerous cells)
• Thoracentesis (a sample of fluid is removed with a needle inserted between the ribs)
• Thoracic CT
• Ultrasound of the chest

Treatment

Treatment may be directed at removing the fluid, preventing it from accumulating again, or addressing the underlying cause of the fluid buildup.

Therapeutic thoracentesis may be done if the fluid collection is large and causing pressure, shortness of breath, or other breathing problems, such as low oxygen levels. Removing the fluid allows the lung to expand, making breathing easier. Treating the underlying cause of the effusion then becomes the goal.

For example, pleural effusions caused by congestive heart failure are treated with diuretics (water pills) and other medications that treat heart failure. Pleural effusions caused by infection are treated with appropriate antibiotics. In people with cancer or infections, the effusion is often treated by using a chest tube for several days to drain the fluid. Chemotherapy, radiation therapy, surgery, or instilling medication into the chest that prevents re-accumulation of fluid after drainage may be used in some cases.

Cutaneous Abnormalities

Cutaneous Abnormalities

Macule -

A small localized change in the color of skin that is neither raised (elevated) nor depressed. Macules are never large. They are basically little spots or blemishes in the skin. They are entirely flat and can only be appreciated by visual inspection; they cannot be seen from the side, just from above.

Papule

A papule is a solid raised lesion that has distinct borders and is less than 1 cm in diameter. Papules may have a variety of shapes in profile (domed, flat-topped, umbilicated) and may be associated with secondary features such as crusts or scales.

Nodule-

A small solid collection of tissue, a nodule is palpable (can be felt). It may range in size from greater than 1.0 cm (3/8 inch) to somewhat less than 2 cm (13/16 inch) in diameter. A nodule may be present in the epidermis, dermis or subcutis (at any level in the skin).

Vesicle:

A vesicle is a circumscribed, fluid-containing, epidermal elevation generally considered less than either 5or 10mm in diameter at the widest point.

Bulla :

A fluid-filled blister more than 5 mm (about 3/16 inch) in diameter with thin walls.

A bulla on the skin is a blister. A bulla on the pleura (the membrane covering the lung) is also called a bleb.

In Latin a bulla was a "bubble, stud or knob." It referred to any rounded protrusion, particularly one that was hollow or cystic.

Cyst:

A cyst is a growth containing liquid that appears inside your body or under your skin.

Pustule

pustule is a small collection of pus in the top layer of skin (epidermis) or beneath it in the dermis. Pustules frequently form in sweat glands or hair follicles. Pus is a mixture of inflammatory cells and liquid.

Scabies

What is scabies?

Human scabies is caused by an infestation of the skin by the human itch mite (Sarcoptes scabiei var. hominis). The microscopic scabies mite burrows into the upper layer of the skin where it lives and lays its eggs. The most common symptoms of scabies are intense itching and a pimple-like skin rash. The scabies mite usually is spread by direct, prolonged, skin-to-skin contact with a person who has scabies.

Scabies occurs worldwide and affects people of all races and social classes. Scabies can spread rapidly under crowded conditions where close body contact is frequent. Institutions such as nursing homes, extended-care facilities, and prisons are often sites of scabies outbreaks.

Transmission

Human scabies is caused by an infestation of the skin by the human itch mite (Sarcoptes scabiei var. hominis). The adult female scabies mites burrow into the upper layer of the skin (epidermis) where they live and deposit their eggs. The microscopic scabies mite almost always is passed by direct, prolonged, skin-to-skin contact with a person who already is infested. An infested person can spread scabies even if he or she has no symptoms. Humans are the source of infestation; animals do not spread human scabies.

Persons At Risk

Scabies can be passed easily by an infested person to his or her household members and sexual partners. Scabies in adults frequently is sexually acquired.

Scabies is a common condition found worldwide; it affects people of all races and social classes. Scabies can spread easily under crowded conditions where close body and skin contact is common. Institutions such as nursing homes, extended-care facilities, and prisons are often sites of scabies outbreaks. Child care facilities also are a common site of scabies infestations.

Symptoms

When a person is infested with scabies mites the first time, symptoms usually do not appear for up to two months (2-6 weeks) after being infested; however, an infested person still can spread scabies during this time even though he/she does not have symptoms.

If a person has had scabies before, symptoms appear much sooner (1-4 days) after exposure. An infested person can transmit scabies, even if they do not have symptoms, until they are successfully treated and the mites and eggs are destroyed.

Common Symptoms

The most common symptoms of scabies, itching and a skin rash, are caused by sensitization (a type of “allergic” reaction) to the proteins and feces of the parasite. Severe itching (pruritus), especially at night, is the earliest and most common symptom of scabies. A pimple-like (papular) itchy (pruritic) “scabies rash” is also common. Itching and rash may affect much of the body or be limited to common sites such as:

• between the fingers,
• wrist,
• elbow,
• armpit,
• penis,
• nipple,
• waist,
• buttocks,
• shoulder blades.

The head, face, neck, palms, and soles often are involved in infants and very young children, but usually not adults and older children.

Tiny burrows sometimes are seen on the skin; these are caused by the female scabies mite tunneling just beneath the surface of the skin. These burrows appear as tiny raised and crooked (serpiginous) grayish-white or skin-colored lines on the skin surface. Because mites are often few in number (only 10-15 mites per person), these burrows may be difficult to find. They are found most often in the webbing between the fingers, in the skin folds on the wrist, elbow, or knee, and on the penis, breast, or shoulder blades.

Medications

• Sulphur has been used since around 25 AD to treat Scabies. You can find bar soap with sulfur in the ranges of 1%-10% to kill scabies, it's recommended you go with 6% or above. Wash whole body once daily for 4 days. It is still recommended that you wash all clothing and bedclothes in hot water and tumble dry on hot as with Permethrin. However, this treatment is largely ineffective.

Topical drugs

• Permethrin 5% is topical medication of choice. Toxicity may resemble allergic reactions. It is usually applied to the skin before bedtime and left on for about 8 to 14 hours, then showered off in the morning. Package directions or doctor's instructions should be followed, but one application is normally sufficient to cure an infection
• Eurax (USP Crotamiton) This is not a cure but helps to relieve itch (pruritis)
• Malathion: Applied for 24 hours; effective in killing both adults and eggs.
• Lindane lotion is approved in the U.S. for use as a second-line treatment where first-line medications like permethrin have either failed, are not well tolerated or otherwise contraindicated It is illegal in 17 other countries, and 33 more countries have restricted its use. Though rare, serious side effects have resulted from product misuse.The FDA has confirmed 3 deaths that all involved use of lindane not in accordance with the label, including excessive topical applications and oral ingestions.
• There is some evidence that a 10% sulfur ointment in petroleum jelly applied topically is effective. It is cheap and readily available over-the-counter. It also has the advantage of being able to be used in pregnant women and infants under two months of age.
• Neem oil is deemed very effective in the treatment of scabies although only preliminary scientific proof exists which still has to be corroborated, and is recommended for those who are sensitive to permethrin, a known insecticide which might be an irritant. Also, the scabies mite has yet to become resistant to neem, so in persistent cases neem has been shown to be very effective.
• Tea tree oil at 5% was only partially effective and does not seem to be a viable solution for treatment. In one study, it was more effective than commercial medications against the scabies mite in an in vitro situation.

Oral

A single dose of Ivermectin has been reported to reduce the load of scabies but another dose is required after 2 weeks for full eradication. In 1999, a small scale test comparing topically applied Lindane to orally administered Ivermectin found no statistically significant differences between the two treatments. As Ivermectin is easily administered (not requiring a rub down of the whole body like lindane or permethrin twice per treatment), compliance is much better. Ivermectin is used in eradication programs of many parasites of both human and animal. Side effects may include mild abdominal pain, nausea, vomiting, myalgia and/or arthralgia, which subside. The product is considered safe for use in children over five months of age.

Public health and prevention strategies

There is no vaccine available for scabies, nor are there any proven causative risk factors. Therefore, most strategies focus on preventing re-infection. All family and close contacts should be treated at the same time, even if asymptomatic. Cleaning of environment should occur simultaneously, as there is a risk of reinfection. Therefore it is recommended to wash and hot iron all material (such as clothes, bedding, and towels) that has been in contact with scabies infestation.

Cleaning the environment should include:

• Treatment of furniture and bedding.
• Vacuuming floors, carpets, and rugs.
• Disinfecting floor and bathroom surfaces by mopping.
• Cleaning the shower/bath tub after each use.
• Daily washing of recently worn clothes, towels and bedding in hot water, drying in a hot dryer and steam ironing.

Itchiness during treatment

Options to combat itchiness include antihistamines such as chlorpheniramine. Prescription: Hydroxyzine (Atarax).

Cholecystitis

Cholecystitis

Cholecystitis is inflammation of the gallbladder, usually resulting from a gallstone blocking the cystic duct.

• Gallbladder inflammation usually results from a gallstone blocking the flow of bile.
• Typically, people have abdominal pain that lasts more than 6 hours, fever, and nausea.
• Ultrasonography can usually detect signs of gallbladder inflammation.
• The gallbladder is removed, often using a laparoscope.

Cholecystitis is the most common problem resulting from gallbladder stones. It occurs when a stone blocks the cystic duct, which carries bile from the gallbladder.

Cholecystitis is classified as acute or chronic.

Acute Cholecystitis: Acute cholecystitis begins suddenly, resulting in severe, steady pain in the upper abdomen. At least 95% of people with acute cholecystitis have gallstones. The inflammation almost always begins without infection, although infection may follow later. Inflammation may cause the gallbladder to fill with fluid and its walls to thicken.

Rarely, a form of acute cholecystitis without gallstones (acalculous cholecystitis) occurs. Acalculous cholecystitis is more serious than other types of cholecystitis. It tends to occur after the following:

• Major surgery
• Critical illnesses such as serious injuries, major burns, and bodywide infections (sepsis)
• Intravenous feedings for a long time
• Fasting for a prolonged time
• A deficiency in the immune system

It can occur in young children, perhaps developing from a viral or another infection.

Chronic Cholecystitis: Chronic cholecystitis is gallbladder inflammation that has lasted a long time. It almost always results from gallstones. It is characterized by repeated attacks of pain (biliary colic). In chronic cholecystitis, the gallbladder is damaged by repeated attacks of acute inflammation, usually due to gallstones, and may become thick-walled, scarred, and small. The gallbladder usually contains sludge (microscopic particles of materials similar to those in gallstones), or gallstones that either block its opening into the cystic duct or reside in the cystic duct itself.

Symptoms of Cholecystitis

The list of signs and symptoms mentioned in various sources for Cholecystitis includes the 21 symptoms listed below:

• Upper right-side abdominal pain
• Biliary colic - spasmodic upper abdominal pain
• Biliary colic after a fatty meal
• Abdominal discomfort
• Pain under right shoulder blade
• Fever
• Nausea
• Vomiting
• Flatulence
• Jaundice
• Itching skin
• Pale stool
• Thickening of gallbladder
• Shrinking of gallbladder
• Gallbladder inflammation
• Back pain
• Indigestion
• Yellow skin
• Yellow membranes
• Yellow whites of the eyes

Diagnosis

Cholecystitis is usually diagnosed by a history of the above symptoms, as well examination findings:

• fever (usually low grade in uncomplicated cases)
• tender right upper quadrant +/- Murphy's sign

Subsequent laboratory and imaging tests are used to confirm the diagnosis and exclude other possible causes.

Ultrasound can assist in the differential.

Differential diagnosis

Acute cholecystitis

• This should be suspected whenever there is acute right upper quadrant or epigastric pain.
  • Other possible causes include:
    • Perforated peptic ulcer
    • Acute peptic ulcer exacerbation
    • Amoebic liver abscess
    • Acute amoebic liver colitis
    • Acute pancreatitis
    • Acute intestinal obstruction
    • Renal colic
    • Acute retrocolic appendicitis

Chronic cholecystitis

• The symptoms of chronic cholecystitis are non-specific, thus chronic cholecystitis may be mistaken for other common disorders:
  • Peptic ulcer
  • Hiatus hernia
  • Colitis
  • Functional bowel syndrome

It is defined pathologically by the columnar epithelium has reached down the muscular layer.

Treatment

People with acute or chronic cholecystitis need to be hospitalized. They are not allowed to eat or drink and are given fluids and electrolytes intravenously. A doctor may pass a tube through the nose and into the stomach, so that suctioning can be used to keep the stomach empty and reduce fluid accumulating in the intestine if the intestine is not contracting normally. Usually, antibiotics are given intravenously, and pain relievers are given.

If acute cholecystitis is confirmed and the risk of surgery is small, the gallbladder is usually removed within 24 to 48 hours after symptoms start. If necessary, surgery can be delayed for 6 weeks or more while the attack subsides. Delay is often necessary for people with a disorder that makes surgery too risky (such as a heart, lung, or kidney disorder). If a complication such as an abscess, gangrene, or perforated gallbladder is suspected, immediate surgery is necessary.

In chronic cholecystitis, the gallbladder is usually removed after the acute episode subsides.

In acalculous cholecystitis, immediate surgery is necessary to remove the diseased gallbladder.

Surgical removal of the gallbladder (cholecystectomy) is usually done using a flexible viewing tube called a laparoscope. After small incisions are made in the abdomen, the laparoscope and other tubes are inserted, and surgical tools are passed through the incisions and used to remove the gallbladder.

Systemic lupus erythematosus

Systemic lupus erythematosus

Systemic Lupus Erythematosus

Systemic lupus erythematosus is a chronic (persistent) disease that causes inflammation in various parts of the body. It is commonly just called SLE or 'lupus'. The severity of SLE ranges from mild to severe. There are two main forms of lupus. Discoid lupus only affects only the skin . The other form is systemic lupus erythematosus which involves the skin and joints and may involve internal organs such as the heart or kidney as well

Pathophysiology

SLE is an autoimmune disorder characterized by multisystem microvascular inflammation with the generation of autoantibodies. Although the specific cause of SLE is unknown, multiple factors are associated with the development of the disease, including genetic, racial, hormonal, and environmental factors.Many immune disturbances, both innate and acquired, occur in SLE, as illustrated in below.

In systemic lupus erythematosus (SLE), many genetic-susceptibility factors, environmental triggers, antigen-antibody responses, B-cell and T-cell interactions, and immune clearance processes interact to generate and perpetuate autoimmunity.

One proposed mechanism for the development of autoantibodies involves a defect in apoptosis that causes increased cell death and a disturbance in immune tolerance.The redistribution of cellular antigens during apoptosis leads to a cell-surface display of plasma and nuclear antigens in the form of nucleosomes. Thus, dysregulated (intolerant) lymphocytes begin targeting normally protected intracellular antigens.

Immune complexes form in the microvasculature, leading to complement activation and inflammation. Moreover, antibody-antigen complexes deposit on the basement membranes of skin and kidneys. In active SLE, this process has been confirmed based on the presence of complexes of nuclear antigens such as DNA, immunoglobulins, and complement proteins at these sites. Serum antinuclear antibodies (ANAs) are found in virtually all individuals with active SLE, and antibodies to native double-stranded DNA (dsDNA) are relatively specific for the diagnosis of SLE.

History

A detailed and accurate history is crucial to aid in diagnosing the type of AKI and in determining its subsequent treatment. A detailed history and a physical examination in combination with routine laboratory tests are useful in making a correct diagnosis .

• Distinguishing AKI from chronic renal failure is important, yet making the distinction can be difficult. A history of chronic symptoms — fatigue, weight loss, anorexia, nocturia, and pruritus — suggests chronic renal failure.
• Take note of the following findings during the physical examination:
  • Hypotension
  • Volume contraction
  • Congestive heart failure
  • Nephrotoxic drug ingestion
  • History of trauma or unaccustomed exertion
  • Blood loss or transfusions
  • Evidence of connective tissue disorders or autoimmune diseases
  • Exposure to toxic substances, such as ethyl alcohol or ethylene glycol
  • Exposure to mercury vapors, lead, cadmium, or other heavy metals, which can be encountered in welders and miners
• People with the following comorbid conditions are at a higher risk for developing AKI:
  • Hypertension
  • Congestive cardiac failure
  • Diabetes
  • Multiple myeloma
  • Chronic infection
  • Myeloproliferative disorder
• Urine output history can be useful. Oliguria generally favors AKI. Abrupt anuria suggests acute urinary obstruction, acute and severe glomerulonephritis, or embolic renal artery occlusion. A gradually diminishing urine output may indicate a urethral stricture or bladder outlet obstruction due to prostate enlargement.
• Because of a decrease in functioning nephrons, even a trivial nephrotoxic insult may cause AKI to be superimposed on chronic renal insufficiency.

Signs and symptoms

Common initial and chronic complaints include fever, malaise, joint pains, myalgias, fatigue, and temporary loss of cognitive abilities. Because they are so often seen with other diseases, these signs and symptoms are not part of the diagnostic criteria for SLE.


Dermatological manifestations

• Malar rash describes an erythematous rash over the cheeks and nasal bridge, with classic nasolabial fold sparing, as seen in the image below.
  

  

  The classic malar rash, also known as a butterfly rash, with distribution over the cheeks and nasal bridge. Note that the fixed erythema, sometimes with mild induration as seen here, characteristically spares the nasolabial folds.

• Photosensitive rash is often macular or diffusely erythematous in sun-exposed areas of the face, arms, or hands, as in the image below.
  
  

  

  Photosensitive systemic lupus erythematosus (SLE) rashes typically occur on the face or extremities, which are sun-exposed regions. Photo courtesy of Dr. Erik Stratman, Marshfield Clinic.

Musculoskeletal manifestations
Joint symptoms, ranging from intermittent joint pains (arthralgias) to sudden inflammation of multiple joints (acute polyarthritis), occur in about 90% of people and may exist for years before other symptoms appear. In long-standing disease, marked joint deformity may occur (Jaccoud's arthropathy) but is rare. However, joint inflammation is generally intermittent and usually does not damage the joints.

Hematological manifestations
Anemia and iron deficiency may develop in up to 50% of cases. Low platelet and white blood cell counts may be due to the disease or a side-effect of pharmacological treatment. People with SLE may have an association with antiphospholipid antibody syndrome(a thrombotic disorder), wherein autoantibodies to phospholipids are present in their serum. Abnormalities associated with antiphospholipid antibody syndrome include a paradoxical prolonged PTT Partial thromboplastin time (which usually occurs in hemorrhagic disorders) and a positive test for antiphospholipid antibodies; the combination of such findings have earned the term lupus anticoagulant-positive. Another autoantibody finding in SLE is the anticardiolipin antibody, which can cause a false positive test for syphilis.

Renal manifestations
Hypertension or hematuria may signal nephritic SLE. Edema of periorbital or peripheral regions and anasarca are common physical findings related to nephrotic syndrome or volume overload with renal failure.

Pulmonary manifestations

Lung and pleura inflammation can cause pleuritis, pleural effusion, lupus pneumonitis, chronic diffuse interstitial lung disease, pulmonary hypertension, pulmonary emboli, pulmonary hemorrhage, and shrinking lung syndrome.

Lymph Node and Spleen Problems

Wide-spread enlargement of the lymph nodes is common, particularly among children, young adults, and blacks of all ages. Enlargement of the spleen (splenomegaly) occurs in about 10% of people. People may experience nausea, diarrhea, and vague abdominal discomfort. The occurrence of these symptoms may be the forewarning of a flare-up.

Nervous System Problems

Involvement of the brain (neuropsychiatric lupus) can cause headaches, mild impairment of thinking, personality changes, stroke, epilepsy, severe mental disorders (psychoses), or a condition in which a number of physical changes may occur in the brain, resulting in disorders such as dementia. The nerves in the body or spinal cord may also be damaged.

Kidney Problems

Kidney involvement may be minor and without symptoms or may be relentlessly progressive and fatal. The most common result of this impairment is protein in the urine that leads to swelling (edema) in the legs.

Blood Problems The numbers of red blood cells, white blood cells, and platelets may decrease. Platelets assist in blood clotting, so if these numbers decrease greatly, bleeding may occur. Also, and for other reasons, the blood may clot too easily, which accounts for many of the problems that can affect other organs (such as strokes and blood clots to the lungs or recurrent miscarriages).

Gastrointestinal Tract Problems

Impairment of blood supply to various parts of the gastrointestinal tract may result in abdominal pain, damage to the liver or pancreas (pancreatitis), or a blockage or tear (perforation) of the gastrointestinal tract.

Pregnancy Problems

Pregnant women have a higher-than-normal risk of miscarriage and stillbirth.

Diagnostic criteria

Some physicians make a diagnosis on the basis of the American College of Rheumatology (ACR) classification criteria. The criteria, however, were established mainly for use in scientific research including use in randomized controlled trials which require higher confidence levels, so some people with SLE may not pass the full criteria.

The American College of Rheumatology established eleven criteria in 1982, which were revised in 1997 as a classificatory instrument to operationalise the definition of SLE in clinical trials. They were not intended to be used to diagnose individuals and do not do well in that capacity. For the purpose of identifying patients for clinical studies, a person has SLE if any 4 out of 11 symptoms are present simultaneously or serially on two separate occasions.

1. Serositis: Pleuritis (inflammation of the membrane around the lungs) or pericarditis (inflammation of the membrane around the heart); sensitivity = 56%; specificity = 86% (pleural is more sensitive; cardiac is more specific).
2. Oral ulcers (includes oral or nasopharyngeal ulcers).
3. Arthritis: nonerosive arthritis of two or more peripheral joints, with tenderness, swelling, or effusion; sensitivity = 86%; specificity = 37%.
4. Photosensitivity (exposure to ultraviolet light causes skin rash, or other symptoms of SLE flareups); sensitivity = 43%; specificity = 96%.
5. Blood—hematologic disorder—hemolytic anemia (low red blood cell count) or leukopenia (white blood cell count<4000/µl), class="mw-redirect">lymphopenia (<1500/µl) sensitivity =" 59%;" specificity =" 89%.Hypocomplementemia is also seen, due to either consumption of C3 and C4 by immune complex-induced inflammation or to congenitally complement deficiency, which may predispose to SLE.
6. Renal disorder: More than 0.5g per day protein in urine or cellular casts seen in urine under a microscope; sensitivity = 51%; specificity = 94%.
7. Antinuclear antibody test positive; sensitivity = 99%; specificity = 49%.
8. Immunologic disorder: Positive anti-Smith, anti-ds DNA, antiphospholipid antibody, and/or false positive serological test for syphilis; sensitivity = 85%; specificity = 93%.Presence of anti-ss DNA in 70% of cases (though also positive with rheumatic disease and healthy persons)^[45]).
9. Neurologic disorder: Seizures or psychosis; sensitivity = 20%; specificity = 98%.
10. Malar rash (rash on cheeks); sensitivity = 57%; specificity = 96%.^[44]
11. Discoid rash (red, scaly patches on skin that cause scarring); sensitivity = 18%; specificity = 99%.

The mnemonic to remember the 11 symptoms is 'SOAP BRAIN MD'.

Some people, especially those with antiphospholipid syndrome, may have SLE without four criteria, and also SLE may present with features other than those listed in the criteria.

Recursive partitioning has been used to identify more parsimonious criteria. This analysis presented two diagnostic classification trees:

1. Simplest classification tree: SLE is diagnosed if a person has an immunologic disorder (anti-DNA antibody, anti-Smith antibody, false positive syphilis test, or LE cells) or malar rash.
   • sensitivity = 92%
   • specificity = 92%
2. Full classification tree: Uses 6 criteria.
   • sensitivity = 97%
   • specificity = 95%

Other alternative criteria have been suggested.

Treatment

Treatment depends on which organs are affected and how active the inflammation of lupus is. The severity of the lupus is not necessarily the same as the activity of the inflammation. For example, organs may be permanently damaged and scarred from lupus that caused inflammation in the past. Such damage may be referred to as “severe,” even if the lupus is not active (that is, it is not causing any inflammation or any further damage at this time). The goal of treatment is to decrease the activity of lupus—that is, to decrease inflammation, which in turn should prevent damage.

If lupus is not very active (sometimes called mild lupus), treatment may not need to be intensive. Nonsteroidal anti-inflammatory drugs (NSAIDs—see Pain: Nonsteroidal Anti-Inflammatory Drugs) often can relieve joint pain. Hydroxychloroquine Some Trade Names
PLAQUENIL
, chloroquine Some Trade Names
ARALEN
, or quinacrine Some Trade Names
ATABRINE
, sometimes taken in combination, helps relieve joint and skin symptoms. Sunscreen lotions (with a sun protection factor of at least 30) should be used, especially by people who have skin rashes.

Very active lupus (sometimes called severe lupus) is treated immediately with a corticosteroid such as prednisone (see Joint Disorders: Corticosteroids: Uses and Side Effects. The dose and duration of treatment depend on which organs are affected. Sometimes an immunosuppressive drug such as azathioprine Some Trade Names
IMURAN
or cyclophosphamide Some Trade Names
LYOPHILIZED CYTOXAN
is given to suppress the body's autoimmune attack. Mycophenolate mofetil Some Trade Names
CELLCEPT
is an alternative immunosuppressive drug. The combination of a corticosteroid and an immunosuppressive drug is most often used for severe kidney disease or nervous system disease and for vasculitis.

Once the initial inflammation is controlled, a doctor determines the dose that most effectively suppresses inflammation over the long term. Usually, the dose of prednisone is gradually decreased when symptoms are controlled and laboratory test results show improvement. Relapses or flare-ups can occur during this process. For most people who have lupus, the dose of prednisone can eventually be decreased or occasionally discontinued.

Surgical procedures and pregnancy may be more complicated for people who have lupus, and they require close medical supervision. Miscarriages and flare-ups during pregnancy are common. Pregnancy should be avoided during a flare-up, and conception should be delayed until the disease seems likely to be inactive.

People who take corticosteroids should be tested periodically and, if necessary, treated for osteoporosis (thinning of the bones), which can occur with chronic corticosteroid use. People should be monitored closely by a doctor for coronary artery disease. Other risk factors for coronary artery disease (for example, high blood pressure and high cholesterol levels) should be controlled as well as possible.

Leprosy

What is leprosy?

Leprosy is a disease caused by the bacteria Mycobacterium leprae that causes damage to the skin and the peripheral nervous system. The disease develops slowly (from six months to 40 years!) and results in skin lesions and deformities, most often affecting the cooler places on the body (for example, eyes, nose, earlobes, hands, feet, and testicles). The skin lesions and deformities can be very disfiguring and are the reason that infected individuals were considered outcasts in many cultures. Although human-to-human transmission is the primary source of infection, three other species can carry and (rarely) transfer M. leprae to humans; chimpanzees, mangabey monkeys, and nine-banded armadillos. The disease is termed a chronic granulomatous disease because it produces inflammatory nodules (granulomas) in the skin and nerves over time.

Child with leprosy

Causes

1. Mycobacterium leprae and Mycobacterium lepromatosis are the causative agents of leprosy.

2. Genetics

Several genes have been associated with a susceptibility to leprosy.

Name	Locus	OMIM	Gene
LPRS1	10p13	609888
LPRS2	6q25	607572	PARK2, PACRG
LPRS3	4q32	246300	TLR2
LPRS4	6p21.3	610988	LTA

Signs and Symptoms and

Unfortunately, the early signs and symptoms of leprosy are very subtle and occur slowly (usually over years). Numbness and loss of temperature sensation (cannot sense very hot or cold temperatures) are some of the first symptoms that patients experience. As the disease progresses, the sensation of touch, then pain, and eventually deep pressure are decreased or lost. Signs that occur, such as relatively painless ulcers, skin lesions of hypopigmented macules (flat, pale areas of skin), and eye damage (dryness, reduced blinking) are experienced before the large ulcerations, loss of digits, and facial disfigurement develop. This long-time developing sequence of events begins and continues on the cooler areas of the body (for example, hands, feet, face, and knees)

Transmission

Researchers suggest that M. leprae are spread person to person by nasal secretions or droplets. They speculate that infected droplets reach other peoples' nasal passages and begin the infection there. Some investigators suggest the infected droplets can infect others by entering breaks in the skin. M. leprae apparently cannot infect intact skin. Rarely, humans get leprosy from the few animal species mentioned above. Routes of transmission are still being researched for leprosy.

Since the disease often appeared in family members, some people thought it was hereditary; other people noted that if there was little or no contact with infected individuals, the disease did not infect others. Consequently, some cultures considered infected people (and occasionally their close relatives) as "unclean" or as " lepers" and ruled they could not associate with uninfected people. Often infected people had to wear special clothing and ring bells so uninfected people could avoid them.

Diagnosis

The majority of cases of leprosy are diagnosed by clinical findings, especially since most current cases are diagnosed in areas that have limited or no laboratory equipment available. Hypopigmented patches of skin or reddish skin patches with loss of sensation, thickened peripheral nerves, or both clinical findings together often comprise the clinical diagnosis. Skin smears or biopsy material that show acid-fast bacilli with the Ziel-Nelson stain or the Fite stain (biopsy) can diagnose multibacillary leprosy, or if bacteria are absent, diagnose paucibacillary leprosy. Other tests can be done, but most of these are done by specialized labs and may help a clinician to place the patient in the more detailed Ridley-Jopling classification and are not routinely done (lepromin test, phenolic glycolipid-1 test, PCR, lymphocyte migration inhibition test or LMIT). Other tests such as CBC test, liver function tests, creatinine test, or a nerve biopsy may be done to help determine if other organ systems have been affected.

Treatment

The majority of cases (mainly clinically diagnosed) are treated with antibiotics. The recommended antibiotics, their dosages and length of time of administration are based on the form or classification of the disease and whether or not the patient is supervised by a medical professional. In general, paucibacillary leprosy is treated with two antibiotics, dapsone and rifampicin, while multibacillary leprosy is treated with the same two plus a third antibiotic, clofazimine. Usually, the antibiotics are given for at least six to 12 months or more. Each patient, depending on the above criteria, has a schedule for their individual treatment, so treatment schedules should be planned by a clinician knowledgeable about that patient's initial diagnostic classification.

Antibiotics can treat paucibacillary leprosy with little or no residual effects on the patient. Multibacillary leprosy can be kept from advancing, and living M. leprae can be essentially eliminated from the person by antibiotics, but the damage done before antibiotics are administered is usually not reversible. Recently, the WHO suggested that single-dose treatment of patients with only one skin lesion with rifampicin, minocycline (Minocin), or ofloxacin (Floxin) is effective. Studies of other antibiotics are ongoing.

The role for surgery in the treatment of leprosy occurs after medical treatment (antibiotics) has been completed with negative skin smears (no detectable acid-fast bacilli) and is often only needed in advanced cases. Surgery is individualized for each patient with the goal to attempt cosmetic improvements and, if possible, to restore limb function and some neural functions that were lost to the disease.

Prevention

In a recent trial, a single dose of rifampicin reduced the rate at which contacts acquired leprosy in the two years after contact by 57%; 265 treatments with rifampicin prevented one case of leprosy in this period. A non-randomized study found that rifampicin reduced the number of new cases of leprosy by 75% after three years.

BCG offers a variable amount of protection against leprosy as well as against tuberculosis.

Stroke

What is a stroke?

A stroke, or cerebrovascular accident (CVA), occurs when blood supply to part of the brain is disrupted, causing brain cells to die. When blood flow to the brain is impaired, oxygen and glucose cannot be delivered to the brain. Blood flow can be compromised by a variety of mechanisms.

Blockage of an artery

• Narrowing of the small arteries within the brain can cause a so-called lacunar stroke, (lacune=empty space). Blockage of a single arteriole can affect a tiny area of brain causing that tissue to die (infarct).
  
  
• Hardening of the arteries (atherosclerosis) leading to the brain. There are four major blood vessels that supply the brain with blood. The anterior circulation of the brain that controls most motor, activity, sensation, thought, speech, and emotion is supplied by the carotid arteries. The posterior circulation, which supplies the brainstem and the cerebellum, controlling the automatic parts of brain function and coordination, is supplied by the vertebrobasilar arteries.

If these arteries become narrow as a result of atherosclerosis, plaque or cholesterol, debris can break off and float downstream, clogging the blood supply to a part of the brain. As opposed to lacunar strokes, larger parts of the brain can lose blood supply, and this may produce more symptoms than a lacunar stroke.

• Embolism to the brain from the heart. In situations in which blood clots form within the heart, the potential exists for small clots to break off and travel (embolize) to the arteries in the brain and cause a stroke.

Rupture of an artery (hemorrhage)

• Cerebral hemorrhage (bleeding within the brain substance). The most common reason to have bleeding within the brain is uncontrolled high blood pressure. Other situations include aneurysms that leak or rupture or arteriovenous malformations (AVM) in which there is an abnormal collection of blood vessels that are fragile and can bleed.

What causes a stroke?

Blockage of an artery

The blockage of an artery in the brain by a clot (thrombosis) is the most common cause of a stroke. The part of the brain that is supplied by the clotted blood vessel is then deprived of blood and oxygen. As a result of the deprived blood and oxygen, the cells of that part of the brain die. Typically, a clot forms in a small blood vessel within the brain that has been previously narrowed due to a variety of risk factors including:

• high blood pressure (hypertension),
  
  
• high cholesterol,
  
  
• diabetes, and
  
  
• smoking.

Embolic stroke

Another type of stroke may occur when a blood clot or a piece of atherosclerotic plaque (cholesterol and calcium deposits on the wall of the inside of the heart or artery) breaks loose, travels through open arteries, and lodges in an artery of the brain. When this happens, the flow of oxygen-rich blood to the brain is blocked and a stroke occurs. This type of stroke is referred to as an embolic stroke. For example, a blood clot might originally form in the heart chamber as a result of an irregular heart rhythm, such as occurs in atrial fibrillation. Usually, these clots remain attached to the inner lining of the heart, but occasionally they can break off, travel through the blood stream, form a plug (embolism) in a brain artery, and cause a stroke. An embolism can also originate in a large artery (for example, the carotid artery, a major artery in the neck that supplies blood to the brain) and then travel downstream to clog a small artery within the brain.

Cerebral hemorrhage

A cerebral hemorrhage occurs when a blood vessel in the brain ruptures and bleeds into the surrounding brain tissue. A cerebral hemorrhage (bleeding in the brain) can cause a stroke by depriving blood and oxygen to parts of the brain. Blood is also very irritating to the brain and can cause swelling of brain tissue (cerebral edema). Edema and the accumulation of blood from a cerebral hemorrhage increases pressure within the skull and causes further damage by squeezing the brain against the bony skull.

Subarachnoid hemorrhage

In a subarachnoid hemorrhage, blood accumulates in the space beneath the arachnoid membrane that lines the brain. The blood originates from an abnormal blood vessel that leaks or ruptures. Often this is from an aneurysm (an abnormal ballooning out of the wall of the vessel). Subarachnoid hemorrhages usually cause a sudden, severe headache and stiff neck. If not recognized and treated, major neurological consequences, such as coma, and brain death will occur.

Vasculitis

Another rare cause of stroke is vasculitis, a condition in which the blood vessels become inflamed.

Migraine headache

There appears to be a very slight increased occurrence of stroke in people with migraine headache. The mechanism for migraine or vascular headaches includes narrowing of the brain blood vessels. Some migraine headache episodes can even mimic stroke with loss of function of one side of the body or vision or speech problems. Usually, the symptoms resolve as the headache resolves.

Risk factors

Overall, the most common risk factors for stroke are:

• high blood pressure,
  
  
• high cholesterol,
  
  
• smoking,
  
  
• diabetes and
  
  
• increasing age.

Heart rhythm disturbances like atrial fibrillation, patent foramen ovale, and heart valve disease can also be the cause.

When strokes occur in younger individuals (less than 50 years old), less common risk factors are considered including illicit drugs, such as cocaine or amphetamines, ruptured aneurysms, and inherited (genetic) predispositions to blood clotting.

An example of a genetic predisposition to stroke occurs in a rare condition called homocystinuria, in which there are excessive levels of the chemical homocystine in the body. Scientists are trying to determine whether the non-hereditary occurrence of high levels of homocystine at any age can predispose to stroke.

What is a transient ischemic attack (TIA)?

A transient ischemic attack (TIA) is a short-lived episode (less than 24 hours) of temporary impairment to the brain that is caused by a loss of blood supply. A TIA causes a loss of function in the area of the body that is controlled by the portion of the brain affected. The loss of blood supply to the brain is most often caused by a clot that spontaneously forms in a blood vessel within the brain (thrombosis). However, it can also result from a clot that forms elsewhere in the body, dislodges from that location, and travels to lodge in an artery of the brain (emboli). A spasm and, rarely, a bleed are other causes of a TIA. Many people refer to a TIA as a "mini-stroke."

Some TIAs develop slowly, while others develop rapidly. By definition, all TIAs resolve within 24 hours. Strokes take longer to resolve than TIAs, and with strokes, complete function may never return andreflect a more permanent and serious problem. Although most TIAs often last only a few minutes, all TIAs should be evaluated with the same urgency as a stroke in an effort to prevent recurrences and/or strokes. TIAs can occur once, multiple times, or precede a permanent stroke. A transient ischemic attack should be considered an emergency because there is no guarantee that the situation will resolve and function will return.

A TIA from a clot to the eye can cause temporary visual loss (amaurosis fugax), which is often described as the sensation of a curtain coming down. A TIA that involves the carotid artery (the largest blood vessel supplying the brain) can produce problems with movement or sensation on one side of the body, which is the side opposite to the actual blockage. An affected patient may experience paralysis of the arm, leg, and face, all on one side. Double vision, dizziness (vertigo), and loss of speech, understanding, and balance can also be symptoms depending on what part of the brain is lacking blood supply.

History

• The American Stroke Association advises the public to be aware of the symptoms of stroke that are easily recognized and to call 911 immediately. These symptoms include the following:
  • Sudden numbness or weakness of face, arm, or leg, especially on one side of the body
  • Sudden confusion, difficulty in speaking or understanding
  • Sudden deterioration of vision of one or both eyes
  • Sudden difficulty in walking, dizziness, and loss of balance or coordination
  • Sudden, severe headache with no known cause
• A focused medical history aims to identify risk factors for atherosclerotic and cardiac disease, including hypertension, diabetes mellitus, tobacco use, high cholesterol, and a history of coronary artery disease, coronary artery bypass, or atrial fibrillation. Consider stroke in any patient presenting with acute neurological deficit or any alteration in level of consciousness. Common signs of stroke include the following:
  • Acute hemiparesis or hemiplegia
  • Complete or partial hemianopia, monocular or binocular visual loss, or diplopia
  • Dysarthria or aphasia
  • Ataxia, vertigo, or nystagmus
  • Sudden decrease in consciousness
• In younger patients, elicit a history of recent trauma, coagulopathies, illicit drug use (especially cocaine), migraines, or use of oral contraceptives.
• Family members, bystanders, and especially prehospital personnel can provide invaluable information regarding the time and events surrounding the onset of symptoms or when the patient was last seen normal.
• Establishing the time the patient was last normal is especially critical when thrombolytic therapy is an option. If the patient awakens with the symptoms, then the time of onset is defined as the time the patient was last seen without symptoms. Family members, coworkers, or bystanders may be required to help establish the exact time of onset, especially in right hemispheric strokes accompanied by neglect or left hemispheric strokes with aphasia.
• If the patient is a candidate for thrombolytic therapy, a thorough review of the inclusion and exclusion criteria must be performed. The exclusion criteria largely focus on identifying risk of hemorrhagic complication associated with thrombolytic use.

Physical

Physical examination is directed toward 5 major areas: (1) assessing the airway, breathing, and circulation (ABCs), (2) defining the severity of the patient's neurologic deficits, (3) identifying potential causes of the stroke (4) identifying potential stroke mimics, and (5) identifying comorbid conditions.

• The physical examination must encompass all the major organ systems, starting with the ABCs and the vital signs. Patients with stroke, especially hemorrhagic, can clinically deteriorate quickly; therefore, constant reassessment is critical. Ischemic strokes, unless large or involving the brainstem, do not tend to cause immediate problems with airway patency, breathing, or circulation compromise. On the other hand, patients with intracerebral or subarachnoid hemorrhage frequently require intervention for both airway protection and ventilation.
  • Vital signs, while nonspecific, can point to impending clinical deterioration and may assist in narrowing the differential diagnosis. Many patients with stroke are hypertensive at baseline, and their blood pressure may become more elevated after stroke. While hypertension at presentation is common, blood pressure decreases spontaneously over time in most patients. Acutely lowering blood pressure has not proven to be beneficial in these stroke patients in the absence of signs and symptoms of associated malignant hypertension, AMI, congestive heart failure (CHF), or aortic dissection.
  • Head, ears, eyes, nose, and throat examination: A careful examination of the head and neck is essential. Contusions, lacerations, and deformities may suggest trauma as the etiology for the patient's symptoms. Auscultation of the neck may elicit a bruit, suggesting carotid disease as the cause of the stroke.
  • Cardiac: Cardiac arrhythmias, such as atrial fibrillation, are found commonly in patients with stroke. Similarly, strokes may occur concurrently with other acute cardiac conditions, such as AMI and acute CHF; thus, auscultation for murmurs and gallops is recommended.
  • Extremities: Carotid or vertebrobasilar dissections, and less commonly, thoracic aortic dissections, may cause ischemic stroke. Unequal pulses or blood pressures in the extremities may reflect the presence of aortic dissections.
• The neurologic examination must be thorough, and yet this is perhaps the weakest area of training for primary care and emergency providers. A directed and focused examination can be performed in minutes and not only provides great insight into the potential cause of the patient's deficits, but also helps determine the intensity of treatment required.
• A useful tool in quantifying neurological impairment is the National Institutes of Health Stroke Scale (NIHSS). This scale easily used, is reliable and valid, provides insight to the location of vascular lesions, and is correlated with outcome in patients with ischemic stroke. It focuses on 6 major areas of the neurologic examination: (1) level of consciousness, (2) visual function, (3) motor function, (4) sensation and neglect, (5) cerebellar function, and (6) language. The NIHSS is used most by stroke teams. It enables the consultant to rapidly determine the severity and possible location of the stroke. A patient's score on the NIHSS is strongly associated with outcome, and it can help identify those patients who are likely to benefit from thrombolytic therapy and those who are at higher risk to develop hemorrhagic complications of thrombolytic use.

Table 1. NIH Stroke Scale (For a printable version, see Media file 1.)

Open table in new window

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Table

	Category	Description	Score
1a	Level of consciousness (LOC)	Alert Drowsy Stuporous Coma	0 1 2 3
1b	LOC questions (month, age)	Answers both correctly Answers 1 correctly Incorrect on both	0 1 2
1c	Answers both correctly Answers 1 correctly Incorrect on both	Obeys both correctly Obeys 1 correctly Incorrect on both	0 1 2
2	Best gaze (follow finger)	Normal Partial gaze palsy Forced deviation	0 1 2
3	Best visual (visual fields)	No visual loss Partial hemianopia Complete hemianopia Bilateral hemianopia	0 1 2 3
4	Facial palsy (show teeth, raise brows, squeeze eyes shut)	Normal Minor Partial Complete	0 1 2 3
5	Motor arm left* (raise 90°, hold 10 seconds)	No drift Drift Cannot resist gravity No effort against gravity No movement	0 1 2 3 4
6	Motor arm right* (raise 90°, hold 10 seconds)	No drift Drift Cannot resist gravity No effort against gravity No movement	0 1 2 3 4
7	Motor leg left* (raise 30°, hold 5 seconds)	No drift Drift Cannot resist gravity No effort against gravity No movement	0 1 2 3 4
8	Motor leg right* (raise 30°, hold 5 seconds)	No drift Drift Cannot resist gravity No effort against gravity No movement	0 1 2 3 4
9	Limb ataxia (finger-nose, heel-shin)	Absent Present in 1 limb Present in 2 limbs	0 1 2
10	Sensory (pinprick to face, arm, leg)	Normal Partial loss Severe loss	0 1 2
11	Extinction/neglect (double simultaneous testing)	No neglect Partial neglect Complete neglect	0 1 2
12	Dysarthria (speech clarity to "mama, baseball, huckleberry, tip-top, fifty-fifty")	Normal articulation Mild to moderate dysarthria Near to unintelligible or worse	0 1 2
13	Best language** (name items, describe pictures)	No aphasia Mild to moderate aphasia Severe aphasia Mute	0 1 2 3
	Total	-	0-42

	Category	Description	Score
1a	Level of consciousness (LOC)	Alert Drowsy Stuporous Coma	0 1 2 3
1b	LOC questions (month, age)	Answers both correctly Answers 1 correctly Incorrect on both	0 1 2
1c	Answers both correctly Answers 1 correctly Incorrect on both	Obeys both correctly Obeys 1 correctly Incorrect on both	0 1 2
2	Best gaze (follow finger)	Normal Partial gaze palsy Forced deviation	0 1 2
3	Best visual (visual fields)	No visual loss Partial hemianopia Complete hemianopia Bilateral hemianopia	0 1 2 3
4	Facial palsy (show teeth, raise brows, squeeze eyes shut)	Normal Minor Partial Complete	0 1 2 3
5	Motor arm left* (raise 90°, hold 10 seconds)	No drift Drift Cannot resist gravity No effort against gravity No movement	0 1 2 3 4
6	Motor arm right* (raise 90°, hold 10 seconds)	No drift Drift Cannot resist gravity No effort against gravity No movement	0 1 2 3 4
7	Motor leg left* (raise 30°, hold 5 seconds)	No drift Drift Cannot resist gravity No effort against gravity No movement	0 1 2 3 4
8	Motor leg right* (raise 30°, hold 5 seconds)	No drift Drift Cannot resist gravity No effort against gravity No movement	0 1 2 3 4
9	Limb ataxia (finger-nose, heel-shin)	Absent Present in 1 limb Present in 2 limbs	0 1 2
10	Sensory (pinprick to face, arm, leg)	Normal Partial loss Severe loss	0 1 2
11	Extinction/neglect (double simultaneous testing)	No neglect Partial neglect Complete neglect	0 1 2
12	Dysarthria (speech clarity to "mama, baseball, huckleberry, tip-top, fifty-fifty")	Normal articulation Mild to moderate dysarthria Near to unintelligible or worse	0 1 2
13	Best language** (name items, describe pictures)	No aphasia Mild to moderate aphasia Severe aphasia Mute	0 1 2 3
	Total	-	0-42

Treatment of ischemic stroke

Ischemic stroke is caused by a thrombus (blood clot) occluding blood flow to an artery supplying the brain. Definitive therapy is aimed at removing the blockage by breaking the clot down (thrombolysis), or by removing it mechanically (thrombectomy). The more rapidly blood flow is restored to the brain, the fewer brain cells die.

Other medical therapies are aimed at minimizing clot enlargement or preventing new clots from forming. To this end, treatment with medications such as aspirin, clopidogrel and dipyridamole may be given to prevent platelets from aggregating.

In addition to definitive therapies, management of acute stroke includes control of blood sugars, ensuring the patient has adequate oxygenation and adequate intravenous fluids. Patients may be positioned with their heads flat on the stretcher, rather than sitting up, to increase blood flow to the brain. It is common for the blood pressure to be elevated immediately following a stroke. Although high blood pressure may cause some strokes, hypertension during acute stroke is desirable to allow adequate blood flow to the brain.