Paracentesis - Procedure Technique

Paracentesis is a procedure to take out fluid that has collected in the abdomen the peritoneal fluid. This fluid buildup is called ascites Ascites may be caused by infection, inflammation, an injury, or other conditions, such as cirrhosis or cancer. The fluid is taken out using a long, thin needle put through the belly. The fluid is sent to a lab and studied to find the cause of the fluid buildup.
Removal and analysis of peritoneal fluid is important in evaluating patients with new onset ascites or ascites of unknown etiology. It is also indicated in patients with known ascites who have a decompensation in their clinical status.

Relative contraindications include

• bleeding diathesis, 
• prior abdominal surgery,
•  distended bowel, or 
• known loculated ascites.

Preparation Before the Procedure; 

• Prior to performing a paracentesis, any severe bleeding diathesis should be corrected.
• Bowel distention should also be relieved by placement of a NG tube, and the bladder should also be emptied before beginning the procedure. 
• If a large-volume paracentesis is being performed, large vacuum bottles with the appropriate connecting tubing should be obtained.

Hyperventilation - Causes And Management

Hyperventilation is breathing which occurs more deeply and/or more rapidly than normal.

Pathophysiology: CO 2 is ‘blown off ’, so that pCO 2 decreases.. Hyperventilation may be primary (‘psychogenic’) or secondary. A classical secondary cause is DKA — Kussmaul’s respiration represents respiratory compensation for a metabolic acidosis.

Secondary causes of hyperventilation
• Metabolic acidosis (eg DKA, uraemia, sepsis, hepatic failure).
• Poisoning (eg aspirin, methanol, CO, cyanide, ethylene glycol).
• Pain/hypoxia.
• Hypovolaemia.
• Respiratory disorders (eg PE, asthma, pneumothorax).

Primary (psychogenic or inappropriate) hyperventilation
Typically, the patient is agitated and distressed with a past history of panic attacks or episodes of hyperventilation. They may complain of dizziness, circumoral paraesthesia, carpopedal spasm, and occasionally sharp or stabbing chest pain. Initial examination reveals tachypnoea with equal
air entry over both lung fields, and no wheeze or evidence of airway obstruction.

Brief Summary of Acute Pulmonary Embolism

Definition:
A pulmonary embolism results from the migration of venous thrombi from the systemic veins to pulmonary arterial system, resulting in varying degrees of obstruction of pulmonary arterial blood flow.
The incidence of pulmonary emboli in the United States exceeds 500,000 per year, with a mortality approaching 10%. If not diagnosed or if improperly treated, the mortality rate can reach 30%.

Common Sources:
Up to 90% of pulmonary emboli originate from the deep venous system of the legs. The upper extremities can also be a source of venous thrombi. Usually related to trauma, congenital fibromuscular bands, or the use of central venous catheters, 12% of all upper extremity thrombi result in pulmonary emboli. In addition, blood clot formation in the pelvic veins may cause either septic or bland pulmonary emboli, especially in the setting of complicated obstetric procedures or gynecologic surgery.
Other causes of pulmonary arterial obstructive emboli include air introduced during intravenous injections, hemodialysis, or the placement of central venous catheters; amniotic fluid secondary to vigorous uterine contractions; fat as a result of multiple long bone fractures; parasites; tumor cells; or injected foreign material (talc, mercury).

Risk Factors:
Three basic risk factors, known collectively as Virchow’s triad, are associated with thrombus formation and subsequent pulmonary emboli:

1. stasis,
2. hypercoagulability, and 
3. endothelial injury.

Management Of Acute Pulmonary Embolism

The goal of therapy is to prevent further embolic episodes, and heparin is the initial drug of choice for accomplishing this. First, a large intravenous loading bolus should be given, followed by continuous-drip infusion, maintained for at least 5 and often 7 to 10 days. Anticoagulation should not be withheld pending the results of further studies unless the patient’s risk of bleeding complications is greater than the clinical suspicion of pulmonary emboli. The partial thromboplastin time should be monitored and the heparin dosage adjusted to keep the time between 1.5 to 2.0 times the control.

Warfarin is started 24 to 48 hours after heparin therapy has been initiated. During the first 3 days of warfarin therapy, the prothrombin time or INR is increased before the onset of true anticoagulation. Therefore, before discontinuing the heparin, the prothrombin time or INR should be therapeutic (1.5 to 2 times normal) for approximately 2 to 3 days.

Low-molecular-weight heparins are indicated for prophylaxis in postoperative patients and probably have a role in the management of acute pulmonary embolism and deep venous thrombosis because they do not require monitoring of the anticoagulation effects.

Continuing the Treatment:
Long-term anticoagulation is usually achieved with warfarin, although low-molecular-weight heparins can also be used. Patients with reversible risk factors that are subsequently eliminated should undergo anticoagulation for a total of 3 months.

Understanding Bone marrow Transplantation

In bone marrow transplantation, usually 500 to 700 ml of marrow is aspirated from the pelvic bones of a human leukocyte antigen (HLA)–compatible donor (allogeneic) or of the recipient himself during periods of complete remission (autologous). The aspirated marrow is filtered and then infused into the recipient in an attempt to repopulate the patient’s marrow with normal cells.
This procedure has effected long-term, healthy survivals in about half of the patients with severe aplastic anemia. Bone marrow transplantation may also be effective in treating patients with acute leukemia, certain immunodeficiency diseases, and solid-tumor cancers.
Because bone marrow transplantation carries serious risks, it requires strict adherence to infection protection techniques and strict aseptic technique. It also requires that a primary caregiver provide consistent care and continuous monitoring of the patient’s status.

Before bone marrow infusion

• Explain to the patient that the success rate depends on the stage of the disease and on finding an HLA-identical sibling match.
• After bone marrow aspiration is completed under local anesthetic, apply pressure dressings to the donor’s aspiration sites. Observe the sites for bleeding. Relieve pain with an analgesic and ice packs as needed.
• Assess the patient’s understanding of bone marrow transplantation. If necessary, correct any misconceptions about the procedure and provide additional information. Prepare the patient to expect an extended facility stay. Explain that chemotherapy and, possibly, radiation therapy are necessary to remove cells that may cause the body to reject the transplant.
• Various treatment protocols are used. For example, I.V. cyclophosphamide may be used with additional chemotherapeutic agents or total body irradiation to suppress the patient’s immune system and requires aggressive hydration to prevent hemorrhagic cystitis. Control nausea and vomiting with an antiemetic (such as ondansetron, prochlorperazine, or metoclopramide) as needed. Give allopurinol, as prescribed, to prevent hyperuricemia resulting from tumor breakdown products. Because alopecia is a common adverse effect of high-dose cyclophosphamide therapy, encourage the patient to choose a wig or scarf before treatment begins.
• Total body irradiation (in one dose or several daily doses) follows chemotherapy, inducing total marrow aplasia. Warn the patient that cataracts, GI disturbances, and sterility are possible adverse effects.

Stomatitis And Other Oral Infections

A common infection, stomatitis—inflammation of the oral mucosa—may extend to the buccal mucosa, lips, and palate. It may occur alone or as part of a systemic disease.

There are two main types: 

1. acute herpetic stomatitis , it is usually short-lived and easily recognized; however, it may be severe in neonates, and potentially fatal.
2. aphthous stomatitis. is common in young girls and female adolescents. It usually heals spontaneously, without a scar, in 10 to 14 days.

Other oral infections include gingivitis, periodontitis, Vincent’s angina, and glossitis.

Causes
Acute herpetic stomatitis results from herpes simplex virus. The cause of aphthous stomatitis is unclear.

Signs and symptoms
Acute herpetic stomatitis begins with burning mouth pain. In immunocompromised individuals, reactivation of the herpes simplex virus infection may be frequent and severe. Gums are swollen and bleed easily, and the mucous membranes are extremely tender. Papulovesicular ulcers appear in the mouth and throat and eventually become punched-out lesions with reddened areolae. The small vesicles rupture and form scales. Another common finding is submaxillary lymphadenitis.
Pain usually disappears from 2 to 4 days before healing of ulcers is complete.
A patient with aphthous stomatitis will typically report burning, tingling, and slight swelling of the mucous membrane. Single or multiple, small round ulcers with whitish centers and red borders appear and heal at one site but then appear at another. The painful stage lasts 7 to 10 days, with healing complete in 1 to 3 weeks.

Special considerations in Patients with Diabetes Mellitus

Special considerations in Patients with Diabetes Mellitus

• Stress that compliance with the prescribed program is essential. Emphasize the effect of blood glucose control on long-term health.
• Watch for acute complications of diabetic therapy, especially hypoglycemia (vagueness, slow cerebration, dizziness, weakness, pallor, tachycardia, diaphoresis, seizures, and coma). Immediately give carbohydrates in the form of fruit juice, hard candy, or honey; if the patient is unconscious, subcutaneous, I.M. or I.V. glucagon or I.V. dextrose may be given.
• Be alert for signs and symptoms of ketoacidosis (acetone breath, dehydration, weak and rapid pulse, Kussmaul’s respirations) and hyperosmolar coma (polyuria, thirst, neurologic abnormalities, stupor). These hyperglycemic crises require I.V. fluids, insulin and, usually, potassium replacement.
• Monitor diabetic control by obtaining blood glucose levels.
• Watch for diabetic effects on the cardiovascular system, such as cerebrovascular, coronary artery, and peripheral vascular impairment, and on the peripheral and autonomic nervous systems.
• Treat all injuries, cuts, and blisters (particularly on the legs or feet) meticulously.
• Be alert for signs of urinary tract infection and renal disease.
• Urge regular ophthalmologic examinations to detect diabetic retinopathy.
• Assess for signs of diabetic neuropathy (numbness or pain in the hands and feet, footdrop, neurogenic bladder). Stress the need for personal safety precautions; explain that decreased sensation can mask injuries. Minimize complications by maintaining strict blood glucose control.

Approach To A Patient Presenting With Chest Pain

Introduction:
Always take chest pain seriously. It may reflect life-threatening illness. Triage patients with chest pain as ‘urgent’ and ensure that they are seen within a few minutes. Ischaemic heart disease is understandably the first diagnosis to spring to mind in the middle-aged or elderly, but chest pain may have a variety of other disease processes, many of which are also potentially life-threatening.

The differential diagnosis of chest pain:

Common causes

• Musculoskeletal (eg costochondritis)
• Acute coronary syndrome
• Pneumothorax
• Oesophagitis
• Pneumonia
• Pulmonary embolism

Less common causes

• Aortic dissection
• Cholecystitis
• Herpes zoster
• Oesophageal rupture
• Pancreatitis
• Vertebral collapse

Reaching the correct conclusion requires accurate interpretation of the history, examination and investigations, bearing in mind recognized patterns of disease presentations.

History

Characterize the pain

• Site (eg central, bilateral or unilateral).

• Severity.

• Time of onset and duration.

• Character (eg ‘stabbing’, ‘tight/gripping’, or ‘dull/aching’).

• Radiation (eg to arms and neck in myocardial ischaemia).

• Precipitating and relieving factors (eg exercise/rest/GTN spray).

• Previous similar pains.

Introduction to Alcoholism

A chronic disorder, alcoholism is usually described as an uncontrolled intake of alcoholic beverages that interferes with physical and mental health, social and family relationships, and occupational responsibilities. Alcoholism cuts across all social and economic groups, involves both sexes, and occurs at all stages of the life cycle, beginning as early as elementary school age. About 20% of patients, even in affluent areas, have alcoholism. Lifetime risk for dependence is 10% to 15% for men and 5% for women.

Causes
Numerous biological, psychological, and sociocultural factors appear to be involved in alcohol addiction. An offspring of one alcoholic parent is seven to eight times more likely to become an alcoholic than is a peer without an alcoholic parent. Biological factors include genetic and biochemical abnormalities, nutritional deficiencies, endocrine imbalances, and allergic responses.
Psychological factors include the urge to drink alcohol to reduce anxiety or symptoms of mental illness; the desire to avoid responsibility in family, social, and work relationships; and the need to bolster self-esteem.
Sociocultural factors include the availability of alcoholic beverages, peer pressure, an excessively stressful lifestyle, and social attitudes that approve of frequent drinking.

Signs and symptoms
Because people with alcohol dependence may hide or deny their addiction and may temporarily manage to maintain a functional life, assessing a patient for alcoholism can be difficult. However, there are various physical and psychosocial symptoms that can facilitate assessment.
The patient’s history may suggest a need for daily or episodic alcohol use to maintain adequate functioning, an inability to discontinue or reduce alcohol intake, episodes of anesthesia or amnesia (blackouts) during intoxication, episodes of violence during intoxication, or interference with social and familial relationships and occupational responsibilities.
Many minor complaints that the patient may have may also be alcohol related. He may mention malaise, dyspepsia, mood swings, depression, or more infections. Note any evidence of an unusually high tolerance for sedatives and narcotics.

Carpal Tunnel Syndrome

The most common of the nerve entrapment syndromes, carpal tunnel syndrome results from compression of the median nerve at the wrist, within the carpal tunnel. This nerve passes through, along with blood vessels and flexor tendons, to the fingers and thumb. Compression neuropathy causes sensory and motor changes in the median distribution of the hand.
Carpal tunnel syndrome usually occurs in women between ages 30 and 60 and poses a serious occupational health problem. Assembly-line workers and packers, secretary-typists, and persons who repeatedly use poorly designed tools are most likely to develop this disorder. Any strenuous use of the hands—ustained grasping, twisting, or flexing—aggravates this condition.

Causes
The carpal tunnel is formed by the carpal bones and the transverse carpal ligament. Inflammation or fibrosis of the tendon sheaths that pass through the carpal tunnel can cause edema and compression of the median nerve.
Many conditions can cause the contents or structure of the carpal tunnel to swell and press the median nerve against the transverse carpal ligament. Such conditions include rheumatoid arthritis, flexor tenosynovitis (commonly associated with rheumatic disease), nerve compression, pregnancy, renal failure, menopause, diabetes mellitus, acromegaly, edema following Colles’ fracture, hypothyroidism, amyloidosis, myxedema, benign tumors, tuberculosis, and other granulomatous diseases. Another source of damage to the median nerve is dislocation or acute sprain of the wrist.

Signs and symptoms
The patient with carpal tunnel syndrome usually complains of weakness, pain, burning, numbness, or tingling in the involved hands. This paresthesia affects the thumb, forefinger, middle finger, and half of the fourth finger. The patient is unable to clench his hand into a fist. The nails may be atrophic; the skin, dry and shiny.
Because of vasodilation and venous stasis, symptoms are usually worse at night and in the morning. The pain may spread to the forearm and, in severe cases, as far as the shoulder. The patient can usually relieve such pain by shaking his hands vigorously or dangling his arms at his side.

Urticaria And Angioedema

Urticaria, commonly known as hives, is an episodic, usually self-limited skin reaction characterized by local dermal wheals surrounded by an erythematous flare. 

Angioedema, which can present either subcutaneously or dermally, produces deeper, larger wheals (usually on the hands, feet, lips, genitals, and eyelids) and a more diffuse swelling of loose subcutaneous tissue. Urticaria and angioedema can occur simultaneously, but angioedema may last longer.

Pathophysiology
Urticaria and angioedema are common allergic reactions. Causes include allergy to drugs, foods, insect stings and, occasionally, inhalants, such as animal dander and cosmetics, that provoke an immunoglobulin (Ig) E-mediated response to protein allergens. However, certain drugs may cause urticaria without an IgE response.
When urticaria and angioedema are part of an anaphylactic reaction, they almost always persist long after the systemic response has subsided. This occurs because circulation to the skin is inhibited after an allergic reaction, which results in slow histamine reabsorption at the reaction site. Nonallergic urticaria and angioedema are probably also related to histamine release.
External physical stimuli, such as cold (usually in young adults), heat, water, or sunlight, may provoke urticaria and angioedema. Dermographism urticaria develops with varying pressure, usually under tight clothing, and is aggravated by scratching.
Several different mechanisms and underlying disorders may provoke urticaria and angioedema. These include IgE-induced release of mediators from cutaneous mast cells; binding of IgG or IgM, resulting in complement activation; localized or secondary infections such as respiratory infection; neoplastic diseases such as Hodgkin’s disease; connective tissue diseases such as systemic lupus erythematosus; collagen vascular diseases; and psychogenic diseases.

Signs and symptoms
The characteristic features of urticaria are distinct, raised, evanescent dermal wheals surrounded by an erythematous flare. These lesions may vary in size. In cholinergic urticaria, the wheals may be tiny and blanched, surrounded by erythematous flares.

Angioedema characteristically produces nonpitted swelling of deep subcutaneous tissue, usually on the eyelids, lips, genitalia, and mucous membranes. These swellings don’t usually itch but may burn and tingle.

Arterial occlusive disease

Introduction: 

With arterial occlusive disease, the obstruction or narrowing of the lumen of the aorta and its major branches causes an interruption of blood flow, usually to the legs and feet. Arterial occlusive disease may affect the carotid, vertebral, innominate, subclavian, mesenteric, or celiac artery. Occlusions, which may be acute or chronic, often cause severe ischemia, skin ulceration, and gangrene.
Arterial occlusive disease is more common in males than in females. The prognosis depends on the location of the occlusion, the development of collateral circulation to counteract reduced blood flow and, if the patient has acute disease, the time elapsed between occlusion and its removal.

Causes
Arterial occlusive disease is a common complication of atherosclerosis. The occlusive mechanism may be endogenous, due to embolus formation or thrombosis, or exogenous, due to trauma or fracture. Predisposing factors include smoking; aging; conditions such as hypertension, hyperlipidemia, and diabetes; and a family history of vascular disorders, myocardial infarction, or stroke.

Signs and symptoms
Evidence of this disease varies widely, according to the occlusion site. (see table at the end of the article)

Diagnosis
With arterial occlusive disease, the diagnosis is usually based on patient history and physical examination.
Pertinent supportive diagnostic tests include the following:

Managing High Blood Pressure

Introduction:
Millions of people around the globe have been diagnosed with high blood pressure or hypertension and it is one of the most common risk factor for stroke and heart attack. High blood pressure can also lead to damage to the blood vessels leading to kidney problems, aneurysms as well as damage to the eyes. It is very important to prevent, control and treat hypertension appropriately.

Guidelines For Target Blood Pressure:

The new guidelines recommend the following target for controlling high blood pressure:

• among adults age 60 and older with high blood pressure, aim for a target blood pressure under 150/90.
• among adults age 30 to 59 with high blood pressure, aim for a target blood pressure under 140/90
• among adults with diabetes or chronic kidney disease, aim for a target blood pressure under 130/80.

Management:Managing high blood pressure involves diet changes, exercise, life style changes and if requires certain medications.

1. Loosing extra weight: Blood pressure often increases as weight increases. Loosing just 10 pounds helps reduces the blood pressure. Beside just loosing weight it is important to keep an eye on the waistline since carrying too much weight around the waistline leads to an increase in blood pressure.

2. Regular Exercise: Exercising regularly has a great impact on preventing and controlling high blood pressure. Even moderate activity for 10 minutes at a time or just walking may alos help a lot.

3. Eating A healthy diet: Aim to eat a diet rich in fruits, vegetables, whole grains and high fiber food. avoid fatty foods and also limit sugar intake.

4. Reduce Sodium In the diet: Even a small reduction of sodium in the diet can help reduce blood pressure greatly. Avoid eating processed food like chips and fast food items that are high in sodium content.

Coronary Artery Disease

Introduction: In the United States, a person dies of coronary heart disease every 39 seconds. Coronary heart disease is a manifestation of atherosclerotic disease and has many modifiable risk factors. Patients with and without coronary heart disease should be advised to stop smoking, maintain normal blood pressure and cholesterol levels, exercise, achieve or maintain a normal weight, and control diabetes mellitus if present.

Pathophysiology: Coronary Heart Disease (CHD) is one of several manifestations of atherosclerotic disease, which begins with endothelium dysfunction.
• Endothelium, when normal, balances vasoconstrictors and vasodilators, impedes platelet aggregation, and controls fibrin production.
• Dysfunctional endothelium encourages macrophage adhesion, plaque growth, and vasoconstriction by recruiting inflammatory cells into the vessel walls, the initiating step of atherosclerosis.
• The vessel wall lesions develop a cap of smooth muscle cells and collagen to become fibroadenomas.
• The vessels with these lesions undergo enlargement, allowing progression of the plaque without compromising the lumen.
• Plaque disruption and thrombus formation, instead of progressive narrowing of the coronary artery lumen, is responsible for twothirds of acute coronary events.
• Plaques most likely to rupture (high-risk plaques) have a large core of lipids, many macrophages, decreased vascular smooth muscle cells, and a thin fibrous cap.
• After plaque rupture, the exposed lipid core triggers a superimposed thrombus that occludes the vessel.
• Increased thrombosis is triggered by known cardiac risk factors including elevated low-density lipoprotein (LDL) cholesterol, cigarette smoking, and hyperglycemia.
• The other one-third of acute coronary events occurs at the site of very stenotic lesions.

Risk Factors: include:
• Family history of premature paternal or sibling myocardial infarction
• Tobacco use and second hand smoke exposure increase the risk of CHD and smoking cessation reduces risk.
• High total cholesterol, high LDL, and/or low high-density lipoprotein (HDL) are independent risk factors.
• Physical inactivity
• Overweight and obesity
• Diabetes mellitus

Allergic Rhinitis - A Brief Discussion

Inroduction: Allergic rhinitis, also known as hay fever, is a type of inflammation in the nose which occurs when the immune system  overreacts to allergens in the air.
Depending on the allergen, the resulting rhinitis and conjunctivitis may be seasonal (hay fever) or year-round (perennial allergic rhinitis). Allergic rhinitis is the most common atopic allergic reaction, affecting over 20 million Americans.

 Causes And Pathophysiology:  Hay fever reflects an immunoglobulin (Ig) E–mediated, type I hypersensitivity response to an environmental antigen (allergen) in a genetically susceptible individual. In most cases, it's induced by wind-borne pollens: in spring, by tree pollens (oak, elm, maple, alder, birch, cottonwood); in summer, by grass pollens (crabgrass, bluegrass, fescue, and ryegrass); and in fall, by weed pollens (ragweed). Occasionally, hay fever is induced by allergy to fungal spores.
With perennial allergic rhinitis, inhaled allergens provoke antigen responses that produce recurring symptoms year-round.
The major perennial allergens and irritants include dust mites, feather pillows, mold, cigarette smoke, upholstery, and animal dander. Seasonal pollen allergy may exacerbate symptoms of perennial rhinitis.

Clinical Features: 
With seasonal allergic rhinitis, the key signs and symptoms are paroxysmal sneezing, profuse watery rhinorrhea, nasal obstruction or congestion, and pruritus of the nose and eyes, usually accompanied by pale, cyanotic, edematous nasal mucosa; red and edematous eyelids and conjunctivae; excessive lacrimation; and headache or sinus pain. Some patients also complain of itching in the throat and malaise.
With perennial allergic rhinitis, conjunctivitis and other extranasal effects are rare, but chronic nasal obstruction is common and often extends to eustachian tube obstruction, particularly in children.