Medical Nursing - Nurses Revision

Osteoarthritis

Osteoarthritis is a type of arthritis that occurs when flexible tissue at the ends of bones wears down.

The wearing down of the protective tissue at the ends of bones (cartilage) occurs gradually and worsens over time.

Therefore, Osteoarthritis can also be defined as a gradual decrease of the cartilage covering of the bone ends within joints.

Osteoarthritis is a degenerative joint disease or sometimes called osteoarthrosis even though inflammation may be present.

It is the most common among the joint disorders and also the most disabling.

Types of Osteoarthritis

Primary Osteoarthritis

it’s the most common and it affects the spine, fingers, hips, knees and great big toes and it has no obvious cause

Secondary Osteoarthritis

occurs with a pre existing abnormality e.g injury or trauma. This can be due to septic arthritis and congenital abnormalities.

Kellgren-Lawrence Classification of Osteoarthritis

grade 0 (none): definite absence of x-ray changes of osteoarthritis
grade 1 (doubtful): doubtful joint space narrowing and possible osteophytic lipping
grade 2 (mild/minimal): definite osteophytes and possible joint space narrowing
grade 3 (moderate): moderate multiple osteophytes, definite narrowing of joint space and some sclerosis and possible deformity of bone ends
grade 4 (severe): large osteophytes, marked narrowing of joint space, severe sclerosis and definite deformity of bone ends

Osteoarthritis is deemed present at grade 2 although of minimal severity

Pathophysiology of Osteoarthritis

Osteoarthritis occurs when the cartilage that cushions the ends of the bone in the joints gradually decreases.
Cartilage is a firm slippery tissue that permits nearly frictionless joint motion. In osteoarthritis, the slick surface of the cartilage becomes rough eventually and if the cartilage wears down completely, bones will be left rubbing onto another bone.
Mechanical injury. OA starts from an injury of the articular cartilage, subchondral bone, and synovium.
Chondrocyte response. Factors that initiate chondrocyte response include previous joint damage, genetic and hormonal factors, and others.
Cytokines. After the chondrocyte response, the release of cytokines occurs.
Stimulation of enzymes. Proteolytic enzymes, metalloproteases, and collagenase are stimulated, produced, and, released.
Damage. The resulting damage predisposes to damage further as the chondrocyte is triggered to respond again.

Cause

Increased age. Most elderly people experience osteoarthritis because the ability of the articular cartilage to resist microfracture with repetitive loads diminishes with age.
Obesity. Obese people easily wear out their weight-bearing joints because of their increased weight.
Previous joint damage. Having previous joint damage predisposes the patient to secondary OA.
Repetitive use. Repetitive use due to occupational or recreational factors also causes OA.

Predisposing Factors

Age. the risk increases with age
Diabetes or other rheumatic diseases
Genetics
Hormonal imbalance
Bone deformities
Increased cholesterol levels
Obesity
Sex more common in females than males
Joint injuries

Signs and Symptoms

Limited movements of the joints
Pain and tenderness
Swelling
Stiffness lasting for a short time after a period of inactivity or when waking up
Crackling noise
Enlarged distorted joints
Bone spurs- these are extra bits of bone which feel like hard lumps may form around the affected joint.

Investigations and Diagnosis

Physical assessment. Physical assessment of the musculoskeletal system reveals the tender and swollen joints.
X-ray. Osteoarthritis characterized by a progressive loss of joint cartilage, which appears on x-ray as a narrowing of the joint space.
Routine blood tests can be useful to exclude infective causes and inflammatory causes.
MRI use of radio waves and strong magnetic fields to produce detailed images of bone and soft tissues including cartilages.
Joint fluid analysis : Use of a needle to draw fluid out of the affected joints. This helps to determine if there is inflammation or if pain is caused by gout or an infection.

Management of Osteoarthritis

Aims

To relief pain
To minimize progress of the condition
To restore normal functions of the bones.

Management according to classification/ severity.

Grade 1- doubtful: patients will develop very minor wear and tear and bone spur growth at the end of the knee joints. Pain and discomfort are rarely felt.

Treatment

If the patient is not predisposed to O.A, orthopedic physicians may not recommend any special treatment
Supplement such as glucosamine may be recommended.
Exercises are also recommended

Grade 2-mild

A diagnostic images or x-rays of the knee joint will show more bone spur growth and through the space between the bones appear normal, people will begin experiencing symptoms of the joint pain. The area around the knee joint will feel stiff and uncomfortable mainly when sitting for a long time or in the morning after waking up after a period of inactivity.

Treatment

non pharmacological therapies to relieve pain and discomfort
exercise and strength training for increased joint stability.
Helping devices

Grade 3- moderate

obvious erosion to the cartilage surface between bones and fibrillation narrow the gap between the bone
Crepitus sounds

Treatment

Over counter NSAIDS or pain relief therapies.
If not effective, doctor may prescribe codeine and oxycodeine.

Supportive treatment

- Physical therapy if it does not work, patient is given articular cortisone.
- Hyaluronic acid over 3-5 weeks time.

Grade 4- Severe

The joint space is reduced causing cartilage to wear off, leaving the joint stiff which leads to a chronic inflammatory response, with decreased synovial fluid that causes friction, greater pain and discomfort when walking or moving the joint.

There is increased production of synovial metalloproteinases, cytokines and TNF(Tumour necrosis factor ) that can diffuse back into the cartilage to destroy soft tissue around the knee.

Treatment.

Incase of severe O.A of the knee, an option is performing osteotomy or bone realignment surgery where the orthopedic surgeon cuts the bone above or below the knee to shorten the length and help realign it for less stress on the joint.
Another surgical option is total knee replacement or arthroplasty.
Arthroplasty. Diseased joint components are replaced in arthroplasty.

Prevention

Weight reduction. To avoid too much weight upon the joints, reduction of weight is recommended.
Prevention of injuries. As one of the risk factors for osteoarthritis is previous joint damage, it is best to avoid any injury that might befall the weight-bearing joints.
Perinatal screening for congenital hip disease. Congenital and developmental disorders of the hip are well known for predisposing a person to OA of the hip.
Keeping a healthy body weight
Reduce on sugar intake.

Complications

Bone death
Bleeding inside the joint
Rapid complete break down of cartilage
Infection of the joint
Rupture of tendons and

Osteoarthritis Read More »

Arthritis

Arthritis is the swelling and tenderness of one or more joints.

Inflammatory arthritis includes a large number of arthritic conditions in which the predominant feature is a synovial inflammation.
This includes post viral arthritis, rheumatic arthritis, seronegative spondyloarthropathy, / arthritis and Lyme arthritis.

Disease presenting as an inflammatory mono arthritis include crystal arthritis e.g. gout, pseudo gout.
Septic arthritis and arthritis due to Juxta – articular bone tumors
Disease presenting as an inflammatory polyarthritis include rheumatoid arthritis, reactive arthritis and Seronegative arthritis associated with psoriasis.

Types of arthritis

Rheumatoid arthritis
Osteoarthritis
Goutily arthritis
Traumatic arthritis
Septic arthritis
Hemophilic arthritis
Gonococcal arthritis
Syphilitic arthritis
Tubercular arthritis

Etiology of arthritis

Trauma
Infection like staphylococci and streptococci
Extrapulmonary TB
Late syphilis
Deposition of crystal like urate crystals in uric acid metabolic disorder arthritis, reactive
Degeneration of articular parts like cartilages
Autoimmunity due to rheumatic fever
Hemorrhage into the joint

Predisposing factor

Gender – women before the menopause are affected three times more often than men
Familial – history
Genetic factors
Age
Renal failure

Rheumatoid Arthritis

Rheumatoid arthritis an autoimmune inflammatory disorder of unknown origin that primarily involves the synovial membrane of the joints

Rheumatoid arthritis is a chronic inflammatory joint condition of un known origin characterized by persistent bilateral proportional small joints involvement resulting in cartilage destruction and bony erosion
with subsequent joint deformities.

The disease affects many systems including articular and non articular structures
It is called seropositive arthritis because of rheumatoid factor that is present in 80% of the cases.
Rheumatology deals with a heterogeneous group of disorder of joint, bones and connective tissues.
Rheumatic diseases affect people of all sexes, ethnic groups, and ages.

The frequency increases with age so that as many as 40% of persons over the age of 50 years have Rheumatic complaints.

Pathophysiology of rheumatoid arthritis

Rheumatoid arthritis is an autoimmune disease where by body tissues are destroyed by its own immune system. The exact cause is not yet known. The disease target the synovium and involves two pathological changes i.e. inflammation and proliferation
The joints are acutely inflamed due to inflammatory changes in the synovial membrane. The synovium becomes thicker, very vascular and the site of increased cell infiltration which may cause an effusion within the joint that manifests as a swollen tender and painful joint with
restriction of its movements. Extra-articular structures lead to rheumatoid nodules (subcutaneous nodules)
The proliferative tissue spreads as pannus over the articular cartilage leading to its slow erosion.

Systemic inflammatory changes can affect many body organs leading to pericarditis, pleuritis, bowel vasculitis, general malaise and anemia
The condition can occur in children less than 16 years as juvenile rheumatoid arthritis or still disease presenting with poly articular arthritis assuming a flexed position, refusing to work, lymphadenopathy, hepatosplenomegaly, pericarditis and pleuritis.

Summary of pathophysiology.

The pathophysiology of rheumatoid arthritis is brief and concise.

Autoimmune reaction. In RA, the autoimmune reaction primarily occurs in the synovial tissue.
Phagocytosis. Phagocytosis produces enzymes within the joint.
Collagen breakdown. The enzymes break down collagen, causing edema, proliferation of the synovial membrane, and ultimately pannus formation.
Damage. Pannus destroys cartilage and erodes the bone.
Consequences. The consequences are loss of articular surfaces and joint motion.
Degenerative changes. Muscle fibers undergo degenerative changes, and tendon and ligament elasticity and contractile power are lost.

Signs and symptoms of rheumatoid arthritis

Joint pain. One of the classic signs, joints that are painful are not easily moved.
Swelling. Limitation in function occurs as a result of swollen joints.
Warmth. There is warmth in the affected joint and upon palpation, the joints are spongy or boggy.
Erythema. Redness of the affected area is a sign of inflammation.
Lack of function. Because of the pain, mobilizing the affected area has limitations.
Deformities. Deformities of the hands and feet may be caused by misalignment resulting in swelling.
Rheumatoid nodules. Rheumatoid nodules may be noted in patients with more advanced rheumatoid arthritis, and they are nontender and movable in the subcutaneous tissue.

Other signs and symptoms include;

Gradual onset of pain and morning stiffness
Loss of appetite and weight
Swelling and progressive loss of joint function
Mild pyrexia and fatigue
Other prodromal signs like anorexia, weakness and vague joint pains that persist for weeks or months followed by pain, tender swollen joints
Inflammation involves three or more joints including small joints
Symmetrical bilateral arthritis involving ankles, knee, wrists, elbows, shoulders, spine and temporomandibular joints
Pain increases with joint movement and may disturb sleep
Subcutaneous nodule
Extra articular manifestation includes splenomegaly, lymphadenopathy, pericarditis, carpal tunnel syndrome, neuropathy, ulcers, pancytopenia and nephritic syndrome
Erythmatous boggy joints
The condition is precipitated by stress, emotions, infections and physical exertion
The condition is characterized by relapses and remissions
There may be hemorrhagic infarcts in the nails and finger pulps.
Inflammation in the eye and ulceration of the white portion of the eye.
Axial joint leading to fetal cervical cord compression.

Assessment and Diagnostic Findings

Physical examination.
History taking.
X-rays of involved joints: Reveals soft-tissue swelling, erosion of joints, and osteoporosis of adjacent bone (early changes) progressing to bone-cyst formation.
Rheumatoid factor (RF): Positive in more than 80% of cases (Rose-Waaler test).
Synovial membrane biopsy: Reveals inflammatory changes and development of pannus (inflamed synovial granulation tissue).
Synovial/fluid aspirate: May reveal volume greater than normal; opaque, cloudy, yellow appearance (inflammatory response, bleeding, degenerative waste products).
Erythrocyte sedimentation rate (ESR): Usually greatly increased (80–100 mm/hr). May return to normal as symptoms improve.
CBC: Usually reveals moderate anemia. WBC is elevated when inflammatory processes are present.
Immunoglobulin (Ig) (IgM and IgG): Elevation strongly suggests autoimmune process as cause for rheumatoid arthritis.
Direct arthroscopy: Visualization of area reveals bone irregularities/degeneration of joint.

Management of rheumatoid arthritis

Aims

To control pain
To prevent joint damage
Control systemic symptoms
Stop inflammation[put disease in remission] wellbeing
Restore physical function and overall
Reduce long term complications
Relieve symptoms

There is no specific cure for Rheumatoid arthritis

Nursing care

Provide adequate rest of the painful swollen joints in acute phase. Use a bed cradle to lift linen from affected joints
Firm back support should be used during the day
The legs must be kept straight and the pillow placed behind the knees, this prevents flexion deformities
Encourage the patient to do active exercise under the guidance of a physiotherapist.
Diet should hence a high protein content with aplenty of milk and eggs
Iron should be given to correct anemia which is common.
Vitamin D, calcium supplements may help to reduce osteoporosis
Should be immobilized in light plastic splints on even plaster of paris.
Relieve pain and discomfort. Provide comfort measures like application of heat or cold massage, position changes, supportive pillows etc
Encourage verbalization of pain. Administer anti inflammatory and analgesic as prescribed.
FACILITATING SELF CARE, Assist patient to identify self care deficit. Develop a plan based on patient perception and priorities.
IMPROVING BODY IMAGE AND COPING SKILLS, Identify areas of life affected by the disease and answer questions., Develop a plan for managing symptoms and enlisting support of family and friends to promote daily function
INCREASING MOBILITY, Asses need for occupational or physical therapy consultation., Encourage independence in mobility and assist as needed
REDUCING FATIGUE, Encourage adherence on treatment programs., Encourage adequate nutrition, Encourage on how to use energy conservation techniques like delegation, setting prioties etc
PROMOTE HOME AND COMMUNITY BASED CARE, Focus on teaching on the disease and possible changes related to it, prescribed drugs and their side effect ., Strategies to maintain independence and safety at home.

MEDICAL MANAGEMENT

There is no cure for rheumatoid arthritis. But recent discoveries indicate that remission of symptoms is more likely when treatment begins early with strong medications known as disease-modifying antirheumatic drugs (DMA). The types of medications recommended will depend on the severity of your symptoms and how long you’ve had rheumatoid arthritis.

NSAIDs. Nonsteroidal anti-inflammatory drugs (NSAIDs) can relieve pain and reduce inflammation. Over-the-counter
NSAIDs include ibuprofen (Advil, Motrin IB) and naproxen sodium (Aleve).
• Acetyl salicylic acid (aspirin) 80 – 100mg/kg daily 4-60
• Other alternative to aspirin, Indomethacin, Naproxen
, Diclofenac Piroxicam. Stronger NSAIDs are available by prescription. Side effects may include ringing in your ears, stomach irritation, heart problems, and liver and kidney damage.
Steroids. Corticosteroid medications, such as prednisone, reduce inflammation and pain and slow joint damage. Side effects may include thinning of bones, weight gain and diabetes. Doctors often prescribe a corticosteroid to relieve acute symptoms, with the goal of gradually tapering off the medication.
Disease-modifying antirheumatic drugs (DMARDs). These drugs can slow the progression of rheumatoid arthritis and save the joints and other tissues from permanent damage. Common DMARDs include methotrexate (Trexall, Otrexup, Rasuvo), leflunomide (Arava), hydroxychloroquine (Plaquenil) and sulfasalazine (Azulfidine). Side effects vary but may include liver damage, bone marrow suppression and severe lung infections.
Biologic agents. Also known as biologic response modifiers, this newer class of DMARDs includes abatacept (Orencia), adalimumab (Humira), anakinra (Kineret), certolizumab (Cimzia), etanercept (Enbrel), golimumab (Simponi), infliximab (Remicade), rituximab (Rituxan), tocilizumab (Actemra) and tofacitinib (Xeljanz). These drugs can target parts of the immune system that trigger inflammation that causes joint and tissue damage. These types of drugs also increase the risk of infections. Biologic DMARDs are usually most effective when paired with a non biologic DMARD, such as methotrexate.

Surgical Management.

SURGERY

If medications fail to prevent or slow joint damage, you and your doctor may consider surgery to repair damaged joints. Surgery may help restore your ability to use your joint. It can also reduce pain and correct deformities.

Rheumatoid arthritis surgery may involve one or more of the following procedures:

Synovectomy. Surgery to remove the inflamed synovium (lining of the joint). Synovectomy can be performed on knees, elbows, wrists, fingers and hips.
Tendon repair. Inflammation and joint damage may cause tendons around your joint to loosen or rupture. Your surgeon may be able to repair the tendons around your joint.
Joint fusion. Surgically fusing a joint may be recommended to stabilize or realign a joint and for pain relief when a joint replacement isn’t an option.
Total joint replacement. During joint replacement surgery, your surgeon removes the damaged parts of your joint and inserts a prosthesis made of metal and plastic.
Osteotomy.
Tenorrhaphy. Tenorrhaphy is the suturing of a tendon.
Arthrodesis. Arthrodesis is the surgical fusion of the joint.
Arthroplasty. Arthroplasty is the surgical repair and replacement of the joint.

Conservative measures

Weight reduction
Joint rest
Avoidance of joint over use
Orthotic devices to support inflamed joints[braces and splits].
Isometric and postural exercises and aerobic exercises
Occupation and physical therapy.

Nursing Diagnosis

Acute and chronic pain related to inflammation and increased disease activity, tissue damage, fatigue, or lowered tolerance level.
Fatigue related to increased disease activity, pain, inadequate sleep/rest, inadequate nutrition, and emotional stress/depression
Impaired physical mobility related to decreased range of motion, muscle weakness, pain on movement, limited endurance, lack or improper use of ambulatory devices.
Self-care deficit related to contractures, fatigue, or loss of motion.
Disturbed body image related to physical and psychological changes and dependency imposed by chronic illness.

Arthritis Read More »

Tendonitis

Tendonitis or Tendinitis

Tendonitis is the inflammation or irritation of a tendon.

Tendinitis can occur in any of your body’s tendons, it’s most common around your shoulders, elbows, wrists, knees and heels.

Anatomy Review

A tendon is a fibrous connective tissue that attaches muscle to bone.

Tendons let us move our limbs. They also help prevent muscle injury by absorbing some of the impact your muscles take when you run, jump or do other movements. Your body contains thousands of tendons.

The tendon plays an extraordinary role in mechanics and movement. They transmit the force produced by the muscular contraction to the skeletal levers, thus allowing the movement and the maintenance of the body posture.

The primary cell types of tendons are the spindle-shaped tenocytes (fibrocytes) and tenoblasts (fibroblasts). Tenocytes are mature tendon cells that are found throughout the tendon structure, typically anchored to collagen fibers. Tenoblasts are spindle-shaped immature tendon cells that give rise to tenocytes. Tenoblasts typically occur in clusters, free from collagen fibers. They are highly proliferative and are involved in the synthesis of collagen and other components of the extracellular matrix.

Tendon sheath is a membrane like structure surrounding the tendon, which separates the tendon from surrounding tissue and allows tendon to glide smoothly inside the sheath.

Tendons are stiffer than muscles, have greater tensile strength and can withstand very large loads with minimal deformations. They differ from ligaments because ligament are fibrous connective tissue that connects bones to other bones and tendinosis – a chronic condition that causes the tendons to break down over time.

Common Types of Tendonitis

Achilles tendonitis is a common sports injury. Additionally, people with rheumatoid arthritis are at a higher risk of Achilles tendinitis.
Tennis elbow – Tennis elbow (lateral epicondylitis) is a painful condition that occurs when tendons in your elbow are overloaded, usually by repetitive motions of the arm and wrist. Wrist tendonitis can affect anyone who repeatedly performs the same movements with their wrists. It is common in people who do a lot of typing, writing, and sports like tennis.
Golfer’s elbow – Medial epicondylitis is also known as golfer’s elbow, baseball elbow, suitcase elbow, or forehand tennis elbow. It’s characterized by pain from the elbow to the wrist on the inside (medial side) of the elbow
Pitcher’s shoulder – When a muscle or tendon is overworked, it can become inflamed. The rotator cuff is frequently irritated in throwers
Swimmer’s shoulder – Swimmer’s shoulder, also called shoulder impingement, is a condition where swimmers often aggravate their shoulders while they swim due to the constant joint rotation. In supraspinatus tendonitis the tendon at the top of the shoulder joint becomes inflamed. This causes pain when moving the arm
Jumper’s knee – Jumper’s knee, also known as patellar tendonitis, is a condition characterized by inflammation of your patellar tendon

Causes of Tendonitis

Tendinitis can be caused by a sudden injury, the condition is much more likely to stem from the repetition of a particular movement over time.

Strain – stretching or tearing of a muscle or a tissue connecting muscle to bone (tendon).
Overuse of the tendons or excessive exercises
Injury or trauma.

Risk factors

Age – in elderly the tendons get less flexible.
Sports and exercises
Diabetes
Rheumatoid arthritis
Antibiotics like quinolones ( Cipro , levofloxacin ) • Trauma or injury

Pathophysiology

The cause of inflammation is irritation of the sheaths by prolonged or abnormal use of the tendons. These sheaths are composed of thin, filmy tissue that permits the sliding motion of tendons within them. Less often it may follow invasion of the tendon sheaths by bacteria with subsequent infection.

Inflammation in the sheath of the tendon produces swelling, redness, and pain along the course of the involved tendon, and motion of the tendon produces severe pain. Swelling of the sheath narrows the space through which the tendon may slide, causing stiffness in the involved area. A grating sensation may be felt as the tendon moves.

Signs and symptoms

★ Redness and Hotness at the site.

★ Pain often described as a dull ache, especially when moving the affected limb or joint. It increases when you move the injured area.

★ Tenderness – The area will be tender, and you’ll feel increased pain if someone touches it.

★ Mild swelling

★ feeling a grating or crackling sensation when you move the tendon

★ Tightness that makes it difficult to move the area

Diagnostic management

Physical examination.
MRI scans to help determine tendon thickening, dislocations and tears
X ray
Ultrasound

Pharmacological / Medical Management

NSAIDs to relieve pain
Platelet-rich plasma (PRP) – PRP treatment involves taking a sample of your own blood and spinning the blood to separate out the platelets and healing factors. The solution is then re-injected into the area of chronic tendon irritation.
Corticosteroid injections to reduce inflammation – Corticosteroids are not recommended for chronic tendinitis (lasting over three months), as repeated injections may weaken a tendon and increase your risk of rupturing the tendon.
Treat underlying conditions like rheumatoid arthritis and diabetes.

Surgical management

For chronic tendon inflammation, focused aspiration of scar tissue (FAST) is a minimally invasive treatment option using ultrasound guidance and very small instruments designed to remove tendon scar tissue without disturbing the surrounding healthy tendon tissue.

Nursing interventions (specific)

★ Enough rest from activities

★ Encourage the patient to use heat or cold therapy as prescribed. Teach the patient to use a barrier between the skin and heat or to use cold therapy to prevent burning or frostbite.

★ Wrapping the area in a compression bandage until swelling subsides

★ Applying heat or ice – Teach the patient how to apply ice and heat properly to prevent burning or chilling.

★ Fluid removal by aspiration and physical therapy to prevent “frozen” joints and preserve motion constitute supplementary treatment

★ Resting or elevating the tendon

★ supports such as splints, braces, or a cane

★ Explain the importance of anti-inflammatory medications, and teach the patient to take them with milk to minimize gastrointestinal (GI) distress.

★ You may be advised to wear a shoe insert that will place your foot in the correct position for walking and running.

★ Physical therapy – Stretching , Massage , Ultrasound , Strengthening exercises

★ Stretches and exercises to build strength and improve mobility in the area

Complications

Contractures (or tightening) of the tendon
Scarring (called adhesions)
Muscle wasting
Disability.

Tendonitis Read More »

Anatomy and Physiology of the Musculo-skeletal System

The muscular-skeletal system is the system that is mainly important in locomotion, body support and makes bodies’ frame work

It consists of skeletal muscles, bones and joints

The skeletal muscle

The muscle consists of bundles of myocytes containing actin and myosin molecules. These molecules integrate and form myofibrils which cause muscle contraction in the same way as myocardial muscle.

Myocyte/sarcomere is elongated surrounded by cell membrane called sarcolemma with nuclei beneath and oxygen binding substance (myoglobin that store oxygen).

Myocyte is surrounded by a connective tissue called endomysium, a group of muscle fibres (fascicle) is surrounded by another connective tissue called perimysium and the whole muscle is surrounded by another connective tissue called epimysium

The three connective tissue forms a tendon which attaches a muscle to the bone surface (enthesis).

A muscle fascia is a fibrous tissue that surrounds the epimysium and tendon

Physiology of a skeletal muscle

Sarcomere is the functional unit of muscle contraction

When a muscle contracts light (actin) filaments and dark (myosin) filaments in a muscle come closer i.e. they interact to shorten the length of the muscle cell.

Many knobs (heads) like projection in myosin form cross-bridges with actin stimulating the muscle to contract, the cross bridge move pulling the filaments pass each other

When the cross bridge has moved as far as it can, it releases the actin and return to original position. The cross bridge is attached to actin of another place

When ATP is absent a muscle is an able to contract continuously (muscle fatigue) leading to muscle cramp.

Control of muscle contraction

The muscle is connected to CNS by motor neuron. Impulses from this neuron contract the muscle.

The point of contact between the motor neuron and muscle is called neuromuscular junction. Vesicle at the axon terminal release acetylcholine an important neurotransmitter

Impulses cause release of calcium ions within the cell which affect regulatory protein that allow actin and myosin to interact and form cross-bridges. A muscle cell will remain in a state of contraction until acetylcholine production stops

Acetylcholinesterase enzyme produced at the neuromuscular junction to destroy acetylcholine that permits re-absorption of calcium into the muscle cell and terminates contraction

Intensity of contraction depends on what you are trying to accomplish. The frontal lobe of the cerebrum decide what and how many muscle cells need to contract

Bones

These form the bodies frame work i.e shape and form of the body They give attachment of muscle and ligaments.
They also protect vital organs, store calcium, form blood elements and allow movement of the body as a whole

The function unit of a bone is an osteocyte

The bony matrix is produced by osteoblasts and comprises of colloids, mineral, carbohydrates and proteins

Various hormones are needed in maintain bony tissue i.e. thyroid hormones, growth hormones, calcitonin, parathyroid hormone and adrenal hormones

Joints

This is where two or more bones met. Joints allow flexibility and movement of the skeleton.

Types of joints

There are three types of joints

Fibrous joints

These are joints in which articulating surfaces of bones are connected by a fibrous tissue. Examples include sutures, middle radioulnar joint and joints between teeth.

There are three types of fibrous joints:

(1) Sutures are nonmoving joints that connect bones of the skull. These joints have serrated edges that lock together with fibers of connective tissue.

(2) The fibrous articulations between the teeth and the mandible or maxilla are called gomphoses and are also immovable.

(3) A syndesmosis is a joint in which a ligament connects two bones, allowing for a little movement (amphiarthroses). The distal joint between the tibia and fibula is an example of a syndesmosis.

Cartilaginous joints

The bone ends are united by a cartilage for example intervertebral joints, pubic symphysis and costochondral joints.

There are two types of cartilaginous joints:

(1) A synchrondosis is an immovable cartilaginous joint. One example is the joint between the first pair of ribs and the sternum.

(2) A symphysis consists of a compressable fibrocartilaginous pad that connects two bones. This type of joint allows for some movement. The hip bones, connected by the pubic symphysis, and the vertebrae, connected by intervertebral discs, are two examples of symphyses.

Synovial joints

These joint articular bony ends are lined by synovial membrane with synovial fluid to permit free movement. These include the ball and socket joints e.g. Hip and the hinge joints e.g. interphalangeal, knee joint etc

Synovial joints are characterized by the presence of an articular capsule between the two joined bones. Bone surfaces at synovial joints are protected by a coating of articular cartilage. Synovial joints are often supported and reinforced by surrounding ligaments, which limit movement to prevent injury. There are six types of synovial joints:

(1) Gliding joints move against each other on a single plane. Major gliding joints include the intervertebral joints and the bones of the wrists and ankles.

(2) Hinge joints move on just one axis. These joints allow for flexion and extension. Major hinge joints include the elbow and finger joints.

(3) A pivot joint provides rotation. At the top of the spine, the atlas and axis form a pivot joint that allows for rotation of the head.

(4) A condyloid joint allows for circular motion, flexion, and extension. The wrist joint between the radius and the carpal bones is an example of a condyloid joint.

(5) A saddle joint allows for flexion, extension, and other movements, but no rotation. In the hand, the thumb’s saddle joint (between the first metacarpal and the trapezium) lets the thumb cross over the palm, making it opposable.

(6) The ball-and-socket joint is a freely moving joint that can rotate on any axis. The hip and shoulder joints are examples of ball and socket joints.

Hyaline cartilage

It forms the articular surface and is vascular. It relies on diffusion from synovial fluid for its nutrition. It is rich in type II collagen that forms a mesh work enclosing giant macro – molecular aggregates or proteoglycans

DISEASES AFFECTING SKELETAL MUSCLES

MYASTHENIA GRAVIS

This is another autoimmune disease predominantly affecting females. There is un usual fatigue due to lack of acetylcholine receptor at the myoneural junctions which impair muscle contraction.

Signs and symptoms

The onset is gradual.
Excessive fatigue particularly towards end of the day with drooping of eye lids
Frequent falls
Difficult in chewing and swallowing
Involvement of respiratory muscles may lead to respiratory failure
A weak cough reflex may lead to accumulation of secretions and infections

Treatment and management

Short acting anticholine esterase drugs like edrophonium
Long acting ant cholinesterase drugs e.g. neostigmine or pyrisostigmine
Thymectomy and steroids also provide relief.
Exercises

MYOSITIS (MYOPATHY)

Myositis or myopathy refers to a group of primary diseases of muscles; Myositis (inflammation of muscles) can be genetically diseases.

Progressive muscular atrophy is a group of hereditary disorder characterized by progressive delegation of muscles without involvement of bones.

The wasting and weakness of muscles is symmetrically without any sensory loss. The affected muscles are large, firm but weak.

The child walks with a waddling giant like that of the duck

When rising from a supine lying position, in bed, the child rolls on his face (prone position) and then uses his arms to push his body up (tripod sign). Death in second decade is usual due to involvement of respiratory muscles.

Fibrositis – rheumatism (fibrocystic)

Fibrositis and muscular Rheumatism are terms used to describe recurring pains, stiffness in the muscles or the back, various parts of the body being involved from time to time.

The disease does not progress and such vague symptoms are attributable to emotional stress.

Treatment

Is usually symptomatic, heat and massages may be helpful and aspirin or one of the NSAIDS can be prescribed.

Anatomy and Physiology of the Musculo-skeletal System Read More »

Hodgkin’s Disease

Hodgkin’s disease

Hodgkin’s disease, also called Hodgkin’s lymphoma, is a type of lymphoma.

LYMPHOMAS

Lymphomas are malignant neoplasms (cancer) of lymphoid tissue.

Lymphoma is a form of cancer that affects the immune system – it is a cancer of immune cells called lymphocytes, a type of white blood cells.

There is abnormal proliferation of lymphatic cells leading to hepatomegaly, splenomegaly and lymphadenitis

Classification of lymphomas

Hodgkin’s lymphoma
Non-Hodgkin’s lymphoma

Hodgkin’s Lymphoma

A malignant proliferation of the lymphoid cells that is characterized histologically by Reed “Sternberg cells.

Hodgkin’s Lymphoma is a malignant disease in which the lymph glands are enlarged and there is an increase of lymphoid tissue in the liver spleen and bone marrow. This disease is fatal if not treated early It was described by a British physician called Thomas Hodgkin in 1832
The exact cause is unknown though it is associated with Epstein Birr Virus (EBV)

Epstein Birr Virus exposure and infection has been linked to its etiology, especially in the under 15 and over 50 age ranges.
It can occur in both sex and ages but more common in male and in the age of 20-35 & 50-70 years (bimodal age distribution)
There is abnormal/neoplastic proliferation of an atypical form of lymphoid cell eponymously termed as reed-sternberg cell. It predominantly a B- cell disease

Clinical staging of Hodgkin’s lymphoma

Stage 1: involvement of a single lymph node or a single extra nodal site

Stage 11: involvement of two or more lymph node regions on the same site of the diaphragm or localized involvement of an extra nodal site and one or more lymph node regions of the same side of the diaphragm

Stage 111: involvement of lymph node region on both sides of the diaphragm

Stage 111 (1): lymphatic involvement of the upper abdomen in the spleen (ophiceliac and portal node)

Stage 111 (2): lymphatic involvement of the upper abdomen in the spleen (ophiceliac and portal node) and the lower abdominal nodes in the periaortic mesenteric and iliac region

Stage IV: diffuse or dissemination of the disease of one or more extra lymphatic organ or tissue with or without lymph node involvement

i.e H- Hepatic, L- lung, P – pleura, M- marrow, D-dermal, and O – osseous

WHO Classification

Nodular sclerosing HL, the most common subtype with large tumor nodules
Mixed cellularity subtype HL is also common subtype
Lymphocyte rich is a rare subtype
Lymphocyte depleted is a rare subtype

Clinical features of Hodgkin’s lymphoma

Enlargement of one or group of nodes which may be discovered following investigation for non specific signs like weight loss (>60% in 6 months), fever and pruritus.

Enlarged lymph nodes are replaced by firm rubbery (elastic character on palpation) pinkish white tissue
Involvement of the spleen, liver and bone marrow if not treated
Lymph node enlargement is insidious
Involved nodes are painless and rubbery in consistency
Fever weight loss, weakness, night sweats and anemia may be present in some cases
Cough and dyspnoea due to enlarged hillar or thoracic lymph nodes
Chills and tachycardia
Hepatosplenomegaly

Abdominal distention and ascites due to enlarged abdominal glands (retroperitoneal nodes)
Patient complain of pain in the affected lymph node after taking alcohol (cause not known)
Dysphagia if mediastinal nodes are involved
Jaundice due to liver involvement
Bone involvement leads to bone pain
Paraplegia due spinal cord compression in extra Dural involvement
Palpable abdominal masses

In advanced stages anemia occur due to decreased erythropoiesis and increase hemolysis

Differential diagnosis

Non-Hodgkin’s lymphoma
Lymphadenitis secondary to TB and cat scratch disease
Pseudo lymphoma caused by phenytoin
Lymphomatoid granulomatosis
Sarcoidosis
HIV disease
SLE

Investigation done in Hodgkin’s lymphoma

Lymph node biopsy
Bone marrow examination
Peripheral blood film reveals normochromic normocytic anemia, eosinophilia, neutrophilia and lymphopenia
Raised ESR
Chest x-ray reveals mediastinal mass
CT-scan of the chest, abdomen and pelvis to define the extent of the disease
Lymphangiography
In TB lymph nodes are large tender, firm and may rapture to for sinuses

Management of Hodgkin’s lymphoma

Radiation therapy for localized disease
Short course combination therapy with less extensive radiation
Radiation is combined with chemotherapy to treat disseminated disease
Cytotoxic drugs are combined with steroids

Two regimens are used i.e
MOPP

Mustin/nitrogen mustard on day 1 and 8

Oncorin/ vincristine day 1 and 8

Procarbazine day 1 and 14

Predisone day I and 14

ABVD

Adriamycin/ dexorubium day 1 and 15

Bleomycin day 1 and 15

Vinblastin day 1 and 15

Decarbazine day 1 and 15

Nursing care is based on pancytopenia (A condition in which there is a lower-than-normal number of red and white blood cells and platelets in the blood.) and other drug effects
Psychological support
Nutrition support
Regular hygiene to prevent infections

NON-HODGKIN’S (NON-BURKITT’S) LYMPHOMA (NHL)

This is cancer that originates from the lymphatic system.

Cancer begins in the cell of the immune system. The disease can begin elsewhere in the lymphatic system but more common found in lymph nodes where by lymphocytes mainly B-cells become abnormal. T-cells can also be affected.

The abnormal cell makes copies which also divide continuously. These cells exceed normal life span and can’t offer defense. Extra cells often form a mass called tumor

There are more than 60 specific non Hodgkin’s lymphomas

Staging of Non Hodgkin disease

The stage depends on how many areas are affected and imaging results

Stage I: The lymphoma cells are in one lymph node group such as in the neck or underarm. Or, if the abnormal cells are not in the lymph nodes, they are in only one part of a tissue or organ (such as the lung, but not the liver or bone marrow).

Stage II: The lymphoma cells are in at least two lymph node groups on the same side of either above or below the diaphragm or, the lymphoma cells are in one part of an organ and the lymph nodes near that organ (on the same side of the diaphragm). There may be lymphoma cells in other lymph node groups on the same side of the diaphragm.

Stage III: The lymphoma is in lymph nodes above and below the diaphragm. It also may be found in one part of a tissue or an organ near these lymph node groups.

Stage IV: Lymphoma cells are found in several parts of one or more organs or tissues (in addition to the lymph nodes). Or, it is in the liver, blood, or bone marrow.

Recurrent: The disease returns after treatment.

In addition to these stage numbers, the disease may also described as stage A or B:

A: You have not had weight loss, drenching night sweats, or fevers

B: You have had weight loss, drenching night sweats, or fevers.

Risk Factors for Non-Hodgkin’s lymphoma/ disease

Weakened immune system: The risk of developing lymphoma may be increased by weak immune system due to inherited condition or certain drugs used after an organ transplant Certain infections such as;

Human immunodeficiency virus (HIV): HIV is the virus that causes People who have HIV infection are at much greater risk of some types of non-Hodgkin lymphoma.
Epstein-Barr virus (EBV): EBV infection is linked to Burkitt
Helicobacter pylori: pylori are bacteria that can cause stomach ulcers increase a person’s risk of lymphoma in the stomach lining.
Human T-cell leukemia/lymphoma virus type 1 (HTLV-1): Infection with HTLV-1 increases a person’s risk of lymphoma and
Hepatitis C virus: Some studies have found an increased risk of lymphoma in people with hepatitis C More research is needed to understand the role of hepatitis C

Age: Although non-Hodgkin lymphoma can occur in young people, the chance of developing this disease goes up with age. Most people with non-Hodgkin lymphoma are older than 60.

Obesity is other possible risk factor for non-Hodgkin lymphoma.

Occupation: People who work with herbicides or certain other chemicals may be at increased risk of this disease.

Clinical features of Non-Hodgkin’s lymphoma

Non-Hodgkin’s lymphoma (NHL) is rare before 40 years.
Lymphadenopathy is common but extra nodal spread occurs early, so first presentation may be in the skin, gut, CNS, or lungs.
Although often symptomless, systemic symptoms are as for HL.
Marrow involvement may cause pancytopenia
Infection is common.
Progressive non tender lymph node enlargement
An unexplained weight loss
Night sweats
Persistent fever
Anemia
Persistent weakness and tiredness
Hepatomegaly
Pain swelling and fullness in the abdomen
Splenomegaly

Diagnosis and Investigation

Physical exam: checking for swollen lymph nodes in the neck, underarms, and groin. Also examine for swollen spleen or liver.

Blood tests: The lab does a complete blood count to check the number of white blood cells. The lab also checks for other cells and substances, such as lactate dehydrogenase (LDH). Lymphoma may cause a high level of LDH.

Chest x-rays: this checks for swollen lymph nodes or other signs of disease in the chest.

Biopsy: A biopsy is taken from lymph node to confirm lymphoma. Removing an entire lymph node is best. The pathologist uses a microscope to check the tissue for lymphoma cells.

Bone marrow biopsy: The doctor uses a thick needle to remove a small sample of bone and bone marrow the hipbone or breast bone. Local anesthesia can help control pain. A pathologist looks for lymphoma cells in the sample.

LFTs and RFTs
Serology tests for HIV

CT scan: An x-ray machine linked to a computer takes a series of detailed pictures of the head, neck, chest, abdomen, or pelvis. A patient is given an injection of contrast material. Also may be asked to drink another type of contrast material. The contrast material makes it easier for the doctor to see swollen lymph nodes and other abnormal areas on the x-ray.

MRI pictures of your spinal cord, bone marrow, or brain. MRI uses a powerful magnet linked to a computer. It makes detailed pictures of tissue on a computer screen or film.

Ultrasound: An ultrasound device sends out micro sound waves. A small hand-held device is held against the patient’s body. The waves bounce off nearby tissues, and a computer uses the echoes to create a picture. Tumors may produce echoes that are different from the echoes made by healthy tissues. The picture can show possible tumors.

Spinal tap: CSF is checked for lymphoma cells or other problems.

PET (positron emission tomography) scan: an injection of a small amount of radioactive sugar is given. A machine makes computerized pictures of the sugar being used by cells in the patient’s body. Lymphoma cells use sugar faster than normal cells and areas with lymphoma look brighter on the pictures. The stage is based on where lymphoma cells are found (in the lymph nodes or in other organs or tissues)

Management of Non Hodgkin’s disease

Specialists who treat non-Hodgkin lymphoma include hematologists, medical oncologists, radiation oncologists, oncology nurses and a registered dietitian. The choice of treatment depends mainly on the following:

The type of non-Hodgkin lymphoma
Stage of lymphoma
How quickly the cancer is growing (whether it is indolent or aggressive lymphoma)
Age of the patient
Other patient’s health problems

1. Watchful waiting:

If a patient has indolent non-Hodgkin lymphoma without symptoms, treatment for the cancer is not initiated immediately. The treatment team watches the patient’s health closely so that treatment can start when symptoms begin
Indolent lymphoma with symptoms needs chemotherapy and biological Radiation therapy may be used for people with Stage I or Stage II lymphoma
In aggressive lymphoma, the treatment is usually chemotherapy and biological therapy People with lymphoma that comes back after treatment may receive high doses of chemotherapy, radiation therapy, or both, followed by stem cell transplantation

Before treatment starts, health care team should explain possible side effects and ways of managing them to the patient

2. Chemotherapy uses drugs to kill cancer cells throughout the body; drug can be administered by oral route, intravenous or into spinal cord in phases depending on the cancer stage and nature of the drug. Drugs in initial stage cyclophosphamide and chlorambucil

In recurrence CDVP (cyclophosphamide, doxorubicin, vincristine and prednisone) or CVPP (cyclophoshamide, vinchristine, procarbozine and prednisone)

Side effects poor appetite, nausea and vomiting, diarrhea, trouble swallowing, or mouth and lip sores, hair loss, infections, bruise or bleeding easily, skin rashes or blisters, headaches, weakness and tiredness

3. Biological therapy:

People with certain types of non-Hodgkin lymphoma may have biological therapy. This type of treatment helps the immune system fight cancer.

Monoclonal antibodies i.e interferon, interlukin 2 and tumor necrosis factor (proteins made in the lab that can bind to cancer cell so that they can be destroyed). Patients receive this treatment through a vein at the doctor’s office, clinic, or hospital.

Flu-like symptoms such as fever, chills, headache, weakness, and nausea may Most side effects are easy to treat. Rarely, a person may have more serious side effects, such as breathing problems, low blood pressure, or severe skin rashes.

4. Radiation therapy/ radiotherapy: uses high-energy rays to kill lymphoma cells. It can shrink tumors and help control Two types of radiation therapy are used for people with lymphoma:

External radiation: A large machine aims the rays at the part of the body where lymphoma cells have collected. This is local therapy because it affects cells in the treated area only. Most people go to a hospital or clinic for treatment 5 days a week for several
Systemic radiation: Some people with lymphoma receive an injection of radioactive material that travels throughout the body. The radioactive material is bound to monoclonal antibodies that seek out lymphoma The radiation destroys the lymphoma cells.
External radiation to abdomen can cause nausea, vomiting, and diarrhea, on chest and neck there may be dry sore throat and difficult in swallowing, the skin may become red, dry, and People who get systemic radiation also may feel very tired, get infections and above signs worsen

5. Stem cell transplantation:

If lymphoma returns after treatment, stem cell transplantation is considered. A transplant of blood-forming stem cells allows a patient to receive high doses of chemotherapy, radiation therapy, or both. The high doses destroy both lymphoma cells and healthy blood cells in the bone marrow. Transplant given through a flexible tube placed in a large vein in the neck or chest area after heavy chemotherapy. New blood cells develop from the transplanted stem cells. The stem cells may come from body of the patient (Autologous stem cell transplantation) or a donor who is a brother, sister or parent (Allogeneic stem cell transplantation) and Syngeneic stem cell transplantation for identical twins

Supportive care aims at controlling pain and other symptoms, to relieve the side effects of therapy and to help the patient cope with the diagnosis. It includes

6. Nutrition: give calories to maintain a good weight, protein to keep promote strength. Eating well may help the patient feel better and have more

7. Activity: Walking, swimming, and other activities can keep the patient strong and Exercise may reduce nausea and pain and make treatment easier to handle. It also can help relieve stress

8. Follow-Up Care: regular checkups after treatment for non-Hodgkin The health team watches patient’s recovery closely and check for recurrence of the lymphoma. Checkups monitors change in health and treatment needs of the patient. Checkups may include a physical exam, lab tests, chest x-rays, and other procedures.

9. Social support: this can be provided by Doctors, nurses, and other members of the health care team who answer many questions about patient’s treatment, working, or other procedures.

Social workers can suggest resources for financial aid, transportation, home care, or emotional support. Support groups like patients or family members meet with other patients or their families to share what they have learned about coping with the disease and the effects of treatment. Groups may offer support in person, over the telephone, or on the Internet. A patient may want to talk with a member of the health care team about finding a support group.

10. Treat treatment side effects appropriately

Helicobacter pylori is treated with antibiotics
Surgical: this corrects stricture and obstruction
Encourage bladder training , habit retraining and intake of oral fluids

Hodgkin’s Disease Read More »

DISEASE OF LYMPH VESSELS

Lymphoedema/lymphatic dysfunction

Lymphoedema refers to swelling in the tissues due to obstruction of lymph drainage

Lymphedema is also defined as the interstitial collection of protein-rich fluid due to disruption of lymphatic flow.

When lymph vessel is obstructed, lymph accumulates in the distal parts leading to low grade inflammation and lymph vessels

Lymphatic dysfunction means that lymphatic system is not working well

Physiologic basis of lymphedema — Lymphedema occurs when the lymphatic load exceeds the transport capacity of the lymphatic system, which causes filtered fluid to accumulate in the interstitium. As opposed to generalized edematous states, the rate of capillary filtration is normal in patients with lymphedema

Causes of lymphoedema

Causes of Lymphoedema can be:

Primary: is due to a congenital and or inherited condition associated with pathologic development of the lymphatic vessels.
Secondary: This occurs as the result of other conditions or treatments

Congenital lymphatic obstruction (Milroy’s disease): failure for the lymph vessel especial in lower limb to develop. This is also called hereditary or primary lymphoedema
Surgical removal of lymph vessel and lymph nodes due to cancer to prevent secondary tumors and further disease spread i.e. removal of axillary nodes during mastectomy may lead to lymphoedema of the affected arm
Tumours can compress lymph vessel blocking lymph flow and tissue drainage
Filariasis: It is a disease caused by tissue dwelling nematode, transmitted by mosquito bite
Malignant metastasis of lymph node and lymph vessel

Signs and symptoms of lymphoedema

Typical signs and symptoms of lymphedema include:

The onset of lymphedema is usually insidious. Affected patients may initially experience aching pain at the affected area and a sense of heaviness or fullness of the limb. Over time, the skin becomes dry and firm with less pitting and is fibrous to palpation.
Two-thirds of cases of lymphedema are unilateral, although the laterality depends on the precipitating event. For example, an axillary node dissection will increase the risk of lymphedema in the ipsilateral arm while a pelvic node dissection increases the risk of bilateral lower extremity edema.
At onset, swelling in the affected limb is typically characterized as “soft” and “pitting”. Pitting is variable in patients with lymphedema and reflects movement of the excess interstitial water in response to pressure. It is generally absent with progressive lymphedema, reflecting the evolution of fibrosis and adipose tissue deposition.
For patients who had previously undergone a lymph node dissection and radiation, lymphedema is typically characterized by slowly progressive ipsilateral swelling of an arm following axillary node dissection or a leg following inguinal node dissection. The swelling may first be apparent only in the proximal portion of the limb, or it can affect only a portion of the distal limb including the digits.
Among patients with breast cancer, there may also be swelling over the ipsilateral breast and/or upper chest wall. Other manifestations include a feeling of heaviness, tightness, aching or discomfort in the limb, and restricted range of motion.
Skin changes — With worsening lymphedema, dermal thickening becomes clinically apparent, which is manifested by cutaneous fibrosis. The overlying skin of the affected limb also becomes hyperkeratotic, which can lead to verrucous and vesicular skin lesions.
Discomfort — A feeling of heaviness, tightness, aching or discomfort in the affected limb commonly accompanies swelling.
Restricted range of motion — With later stages of lymphedema, patients may develop restricted range of motion in the affected limb as a result of the increased weight, which may limit their ability to perform activities of daily living (ADLs).

Summary of Clinical Features

Swelling in arms and legs
Tissues of the neck and head may be affected also.
Reduced mobility due to swelling
Heaviness of the affected area
Skin changes i.e discoloration
Blister formation
Leaking of fluid from the skin
Infections
Poor vision, ear pain and nasal congestion in case of head and neck lymphoedema
Difficult in swallowing
Difficulty in breathing and talking
Salivating
Lymphangitis and cellulitis occur as complications which presents as streaky red patch on area affected, fever, chills and itching

Diagnosis and Investigation of lymphoedema

History: Components of history that should be addressed include:

Age of onset
Area(s) of involvement
Associated symptoms (e.g., pain)
Medications — While none is directly associated with an increased risk of lymphedema, some are associated with edematous states (e.g., NSAIDs agents) or are contraindicated in the treatment of lymphedema (e.g., diuretics)
Progression of symptoms
Past medical history, including of medical conditions associated with lymphedema, any prior travel, infections, surgery or prior RT
Family history

2. Physical Examination.

The physical exam should evaluate the vascular system, skin, and soft tissue, and palpation of the lymph nodes.

If primary lymphedema is suspected, evaluation should include documentation of any physical signs or congenital anomalies associated with an inherited condition. Examples include:

Short stature (Turner Syndrome)
Port wine stains or hemangiomas (Klippel-Trenaunay-Weber Syndrome)
Shield chest (Turner Syndrome, Noonan Syndrome)
A positive Stemmer sign is indicative of lymphedema. It is characterized by the examiner’s inability to lift the skin of the affected limb compared to the contralateral limb. It is also described as difficulty lifting the skin of the dorsum of the fingers or toes of the affected limb. A positive Stemmer sign can be found in any stage of lymphedema. While it is possible to have a false negative Stemmer sign, a false positive sign is rare.
Opto electronic volume try — Volume can be assessed utilizing an infrared, optoelectronic measurements. This technique utilizes infrared beams to scan the limb and calculate a volume.
Circumferential measurements — Circumferential measurements on the affected and contralateral arm are a simple and inexpensive method to estimate edema. Measurements can be taken at any point in the arm or leg, or circumferentially around the head, neck, or trunk, as long as the clinician is utilizing anatomic landmarks to reproduce the measurements. Measurements in the arm are made at four points in both the affected and contralateral arm:
Metacarpal-phalangeal joints
Wrists
Ten centimeters distal to the lateral epicondyles
Fifteen centimeters proximal to the lateral epicondyles
Water displacement detects changes in volume of less than 1 percent. For patients with limb lymphedema, volume difference of 200 mL or more between the affected and opposite limbs is typically considered as a cutoff point to define lymphedema.
Bioimpedance spectroscopy — Bioimpedance spectroscopy (BIS) is a reliable and accurate tool to determine volume. Using electrical current, resistance measurements are used to compare the composition of fluid compartments.

4. Imaging

Computed tomography (CT) scan can demonstrate accumulation of fluid within soft tissue with good sensitivity
MRI has also been used in the evaluation of lymphedema.
Lymphoscintigraphy — Lymphoscintigraphy is a technique used to image the flow of fluid from the skin to the lymph nodes, particularly in the extremities.
X-ray of lymphatic system by introducing a dye between toes or in the groin
Genetic testing — For patients diagnosed with primary lymphedema or suspected of lymphedema tarda, referral to a medical geneticist or genetic counselling service is suggested for evaluation of the family history and recommendations for further work-up.
Blood smear to isolate filarial worms

Stages of Lymphedema.

Staging — Lymphedema is staged using the criteria of the International Society of Lymphology. It involves two criteria to diagnose and classify lymphedema: the “softness” or “firmness” of the limb (reflecting fibrotic soft tissue changes) and the outcome after elevation:

Stage 0 — Stage 0 lymphedema is a subclinical or latent condition where swelling is not evident despite impaired lymphatic transport. Most patients are asymptomatic, but some report a feeling of heaviness in the limb. Stage 0 may exist for months or years before the onset of overt lymphedema occurs (stage I to III).
Stage I – There is accumulation of fluid that subsides with 24-hour limb elevation. The appearance is that of soft edema that may pit, with no evidence of dermal fibrosis. This is sometimes called reversible edema.
Stage II – Stage II lymphedema does not resolve with 24-hour limb elevation alone. This reflects the evolution of dermal fibrosis. As the fibrosis progresses, the limb may no longer pit on examination. This is sometimes called spontaneously irreversible lymphedema.
Stage III – Stage III lymphedema is characterized by lymphostatic elephantiasis. On exam, pitting is absent, and the skin reveals trophic skin changes such as fat deposits, acanthosis, and warty overgrowths.

Classification of lymphedema

Several classification systems are used, including the American Physical Therapy Association (APTA) & National Cancer Institute’s Common Terminology Criteria for Adverse Events (CTCAE). Of these, we prefer the APTA classification system. Both schemas are described below.

APTA uses girth as an anthropometric measurement to classify lymphedema. The maximum girth difference between the affected and unaffected limb is used to determine the class of lymphedema. See ‘Circumferential measurements‘ below):

Mild lymphedema — maximum girth difference <3 cm
Moderate lymphedema — 3 to 5 cm difference
Severe lymphedema — difference >5 cm

National Cancer Institute Common Terminology Criteria for Adverse Events (CTCAE) — categorizes lymphedema based upon exam findings & the presence of functional impairment:

Grade 1 — Trace thickening or faint discoloration
Grade 2 — Marked discoloration; leathery skin texture; papillary formation; limiting instrumental activities of daily living (ADL)
Grade 3 — Severe symptoms limiting self care ADL

Management of lymphoedema

Compression of the affected limb to promote lymph drainage
Wrapping the affected limb in elastic bandage to maintain continuous pressure on swollen limb to reduce the size and improve mobility
Use of compression garments (special designed socks), stockings, or sleeves that have a comfortable fit over the swollen limb (manual lymphatic drainage/lymphatic drainage massage)
Exercise can help fluid move from the vessels and reduce on swelling such as knee bending, wrist rotation, swimming, walking, etc for 20 to 30 minutes daily
Routine skin care
Liposuction in advanced stages of lymphedema when other options fail
Anti biotic are prescribed prevent spread of infections
Treat secondary fever with analgesics
Ensure good diet to improve immunity
Lymphatic venous anastomosis
Massaging
Elevation
Apply pressure on the affected areas
Complete decongestive therapy
Surgery due to obstruction

Lymphangitis

Lymphangitis refers to inflammation of lymph vessels due bacterial infection.

Microbes in the lymph, draining the area infected, spread along the walls of lymph vessel. This may be stopped in the first lymph node or continue involving whole lymph drainage network to even blood.

Potential pathogens include

bacteria,
mycobacteria,
viruses,
Fungi
parasites.

Lymphangitis commonly develops after cutaneous inoculation of microorganisms into the lymphatic vessels through a skin wound or as a complication of a distal infection.

Pathophysiology of Lymphangitis

The major function of the lymphatic system is to resorb fluid and protein from tissues and extravascular spaces. The absence of a basement membrane beneath lymphatic endothelial cells affords the lymphatic channels a unique permeability, allowing resorption of proteins that are too large to be resorbed by venules.
Lymphatic channels are situated in the deep dermis and subdermal tissues parallel to the veins and have a series of valves to ensure one way flow. Lymph drains via afferent lymphatics to regional lymph nodes and then by efferent lymphatics to the cisterna chyli and the thoracic duct into the subclavian vein and venous circulation.
Lymphangitis develops after cutaneous inoculation of microorganisms that invade the lymphatic vessels and spread toward the regional lymph nodes. Organisms may invade lymphatic vessels directly through a skin wound or an abrasion or as a complication of a distal infection.

Pathophysiology of Edema

Circulation of lymph is a complex process. All body tissues are bathed in interstitial fluid and when in excess, it accumulates leading to oedema.

Therefore edema occur due to;

Excessive production of interstitial fluid as in increased capillary permeability due to inflammation, colloid osmotic pressure in hypoproteinemia, high venous pressure in thrombosis
Inadequate removal/ transport of interstitial fluid by lymphatic system lead to accumulation of interstitial fluids a condition called lymphoedema

Normally 2-4 liters of interstitial fluids is filtered per day and is returned to vascular circulation. Fluid flux across capillary depend on hydrostatic and oncotic pressure (positive in arterial end and negative in the venular end)

Causes

Extremity oedema is due to right sided heart failure, constrictive pericarditis, renal diseases, liver cirrhosis and hypoproteinemia
Acute or chronic obstruction in the venous system
Abnormalities in lymphatic system
Allergic disorders

Clinical Manifestation of Lymphangitis

Characterized by erythematous streaks with pain and rapid spread, or by nodular swellings along the course of the lymphatic vessels.

Acute lymphangitis – occur in skin abrasion with infection at a distal site, such as interdigital dermatophyte infection or cellulitis of the lower leg. This may be accompanied by lymphangitis with red, tender streaks extending proximally with involvement of regional lymph nodes (lymphadenitis). Fever may also be present as a systemic symptoms.
In individuals with normal immunity the cause is Streptococcus pyogenes; can also occur in Staphylococcus aureus infection. In immunocompromised patients, gram-negative organisms are important causes of lymphangitis following lower limb cellulitis.
Pasteurella multocida from dog and other animal bites can result in localized infection with concomitant lymphangitis. It occurs in up to 30 percent of Erysipelothrix infections, a zoonosis occurring in persons in contact with fish and some animals. Cutaneous anthrax can present with extensive edema, regional lymphadenopathy, and lymphangitis.
Lymphangitis associated Rickettsiosis has been described with the causative organism R. sibirica mongolotimonae and in African tick bite fever due to R. africae. The presence of an inoculation eschar suggests tick-transmitted infection.
Nodular lymphangitis
- Nodular lymphangitis (also known as sporotrichoid lymphangitis, sporotrichoid spread, or lymphocutaneous syndrome) presents as painful or painless nodular subcutaneous swellings along the course of the lymphatic channels.
- Sporotrichosis has been described in the setting of gardening trauma or injury due to a thorn or wood splinter. It can have an incubation period of up to three months and presents in a cutaneous or a lymphocutaneous form accompanied by lymphangitis; painless ulcers may also be observed. Lesions on the upper limbs are the most common presentation
- lesions may ulcerate with accompanying regional lymphadenopathy. The incubation period between exposure and the onset of nodular lymphangitis can be prolonged and the presentation may be indolent with few or no systemic symptoms.
- Causes of nodular lymphangitis include: Sporothrix schenckii, Nocardia (most often N. brasiliensis), M. marinum, leishmaniasis, tularemia, and systemic mycoses:
- M. marinum has been described to cause “fish tank granuloma,” an entity that can occur following a hand injury while cleaning a fish tank. It has an incubation period of up to eight weeks. Infection due to rapidly growing mycobacteria can also occur in the setting of thorn or splinter injury. Other mycobacterial causes of lymphangitis include M. kansasii, M. chelonae, and M. fortuitum.
- Nocardia infections may present with cutaneous, subcutaneous, or lymphocutaneous manifestations following traumatic injury. Although this may mimic the appearance and clinical course of acute staphylococcal or streptococcal infection, the clinical course is usually much more indolent.
- Cutaneous leishmaniasis can present with subcutaneous nodules with lymphangitis or lymphadenitis up to 24 weeks following exposure. This presentation is more frequent with New World leishmaniasis caused by L. braziliensis or L. mexicana than with Old World Leishmaniasis due to L. major or L. tropica.
- Nodular lymphangitis is a rare manifestation of Francisella tularensis and Burkholderia pseudomallei infection. The initial skin lesion of F tularensis infection may be a papule or an ulcer or contain an eschar. The systemic mycoses, including coccidioidomycosis, blastomycosis, and histoplasmosis, can present with nodular lymphangitis.
- Filarial lymphangitis — The presence of the parasite within the lymphatic channels causes inflammation and subsequent dilatation, thickening, tortuosity of the lymphatic channels with valvular incompetence. Often occurs in a retrograde progression with distal or peripheral spread away from the regional lymph nodes where the adult parasite resides. It can also occur as a result of inflammation due to dying parasites.
- Wuchereria bancrofti, B. malayi, and B. timori are the causes of lymphangitis due to lymphatic filariasis.

Diagnosis of Lymphangitis.

Clinical features, & laboratory analysis of clinical specimens.

Microbiological investigations

Swab, aspirate, and biopsy of the primary site, nodule, or distal ulcer for histology and microscopy (including gram, fungal and acid fast staining), as well as culture (including bacterial, fungal, and mycobacterial cultures).
Serology (e.g., F. tularensis, Histoplasma)
Blood film (e.g., filaria)
Imaging —Lymphangiography (using dye injection into the lymphatics) and lymphoscintigraphy (using intradermal technetium injection at distal site of affected limb) have been used to evaluate for lymphedema and lymphatic obstruction . This may be useful if surgical management of lymphedema is a consideration.

Treatment of Lymphangitis

Some cases of nodular lymphangitis require surgical debridement. In the setting of lymphedema with significant lymphatic obstruction, surgical intervention may also be appropriate. Pending diagnostic evaluation, empiric antibiotic therapy with activity against skin flora may be initiated.

DISEASES OF LYMPH NODES

Lymphadenitis/adenitis

Lymphadenitis refers to inflammation of lymph nodes due bacterial infection spreading from infected lymph vessels.

The lymph nodes become enlarged, tender, congested with blood and chemotaxins.

If the phagocytes and antibody production is overwhelmed abscess may form with in the node Neighboring tissues may become involved and infected materials may be transported to other nodes and blood

Lymphadenititis may be acute or chronic. In children cervical lymph nodes are more affected

Causes of acute lymphadenititis

Measles Typhoid
Cat-scratch fever Wound
Skin infections

Causes of chronic lymphadenititis

TB
Syphilis
Unresolved acute infections

Signs and symptoms of lymphadenitis

Tenderness of the affected nodes
Redness of the skin around the affected nodes
Fever in severe cases

Lymphadenopathy

This refers to enlargement of lymph nodes.

Causes of Lymphadenopathy

It may be local or generalized

Causes of generalized lymphadenopathy include;

Infection like TB, HIV, syphilis
Acute and chronic lymphoid leukemia
Lymphoma like Hodgkin’s and Non-Hodgkin’s lymphoma
Sarcoidosis

Causes of localized lymphadenopathy include

Localized infection ie scalp infection leads to cervical lymph nodes enlargement,
infection of the upper extremity lead to axillary lymph nodes enlargement, infection of the lower limbs lead to inguinal lymph nodes enlargement and infection of the throat or tonsils lead to mandibular lymph node enlargement
Carcinoma that spread to lymphatics lead to regional lymphadenopathy i.e. stomach cancer lead to supraclavicular lymphadenopathy, breast cancer lead to axillary lymphadenopathy.

DISEASES OF THE SPLEEN

Splenomegaly/ hypersplenism

Splenomegaly refers to enlargement of the spleen more than its normal size (12x 7 cm).

The enlarged spleen may be non palpable but it is detectable on scan. It becomes palpable only when enlarged more than two and half times its normal size.

The spleen may be infected by blood-borne microbes or local spread of infection Enlargement of the spleen is associated with problems which include;

Premature destruction of red blood cells
Sequestration of red cells, white cells and platelets (pancytopenia)
Valunabirity to traumatic rapture
Hyperplasia of bone marrow follows as a compensatory response

Causes of splenomegaly

Bacterial infection like endocarditic, tuberculosis, septicemia, brucellosis, syphilis and typhoid
Viral infection like hepatitis and AIDS
Protozoa infection like malaria, leishmaniasis and trypanosomiasis
Fungal like histoplasmosis
Inflammatory disorders like SLE, rheumatoid arthritis and sarcoidosis
Congestion due to portal hypertension, hepatic vein thrombosis, chronic CCF and pericardial effusion
Hemolytic disorders like sickle cell anemia and spherocytosis
Infiltrative diseases of the spleen like leukemia and lymphomas
Iron deficiency anemia and megaloblastic anemia
Idiopathic

Signs and symptoms of splenomegaly

Palpable spleen Fever
Jaundice
Other signs of underlying disease

Management of splenomegaly

Investigations helps in identifying the cause such as blood smear, CBC, radiological imaging and culture and biopsy.
Treat the cause accordingly
In severe persistent spleenism, splenectomy may be performed

Hyposplenism

This refers to lack or impairment of spleen function.

It is due to Trauma
Surgical removal of the spleen
Autoplenectomy as in sickle cell due to ischemic atrophy (microvascular occlusion) Splenic atrophy in celiac disease

Signs of hypoplenism

Recurrent bacterial infection such as streptococci, E-coli, Haemophilus influenza and Neisseria meningitides
Severe septicaemia Intravascular coagulation Multiorgan failure
Red cell abnomalities

DISEASE OF LYMPH VESSELS Read More »

Anatomy and Physiology of the Lymphatic System

ANATOMY AND PHYSIOLOGY OF LYMPHATIC SYSTEM

The lymphatic system is part of the circulatory system which begins with very small close ended vessels called lymphatic capillaries which is in contact with the surrounding tissues and interstitial fluid. The lymphatic system is almost a parallel system to the blood circulatory
system.

It consist of:

Lymph
Lymph vessel
Lymph nodes
Diffuse lymphoid tissue
Bone marrow

Lymph

This is a clear watery fluid which transports plasma proteins, bacteria, fat from ileum and damaged tissues to the lymph nodes for destruction which circulates in lymph vessels.

It has similar composition as plasma and contains lymphocytes and macrophages for defense.
Lymph is an ultra filtrate of blood from capillary ends due to pressure in the blood vessel into the tissue as interstitial fluid totaling approximately 2 liters (1 – 3 % of body weight). Lymph is identical to interstitial fluid

Lymph vessels/Lymphatics

They are similar to blood vessels and its where lymph circulates before it is returned to general blood circulation. They continue from lymph capillaries which originate as blind-ended tube in the interstitial spaces and join lymph nodes, tissues and organs

Lymph capillaries are anatomically similar to blood capillaries i.e. made of a single layer of endothelial cell except there is no basement membrane making them able to allow large molecules like plasma protein that leak into interstitial spaces pass through capillary cells

All body tissues have a network of lymphatic vessels except the brain, spinal cord, bones, conea of the eye and superficial layer of the skin.

Lymph vessles become larger as they join together eventually forming two large ducts that is;

Thoracic duct from cistern chyli in front of L1 & L2 draining lymph from legs, pelvis, abdomen, left of the chest, neck and left arm into the left subclavian vein in root of the neck
Right lymphatic duct in the root of the neck draining lymph from right chest, head, neck and right arm into right subclavian vein

Lymph circulation

The lymphatic system represents an accessory route through which fluid can flow from the interstitial spaces into the blood. The lymphatic’s can carry proteins and large particulate matter away from the tissue spaces.

This returns proteins to blood from the interstitial spaces and is an essential function, without this death occurs within about 24 hours.

Lymph flow is aided by;

Contraction of surrounding skeletal muscles
Movement of the parts of the body
Pulsations of arteries adjacent to the lymphatic
Compression of the tissues by objects outside the body
Rhythmic contraction of lymph large vessels

The lymphatic pump becomes very active during exercise, often increasing lymph flow. Conversely, during periods of rest, lymph flow is sluggish, almost zero.

Lymph nodes

These are oval bean-shaped organs that lie along the lymph vessel. Four or five afferent lymph can vessel enters one lymph node but leave through one vessel. Lymph passes to around 8 nodes before it returns to blood circulation

Lymph nodes consist of lymph tissue which is parked with lymphocytes and macrophages & reticular tissue that produce a network of fibers which provide internal structure with in the node

Large Lymph nodes are located in strategic positions in the body throughout the body arranged in deep and superficial groups’ i.e.

Cervical Lymph nodes drain lymph from the head and neck
Axillary Lymph nodes drain lymph from the upper limbs
Hillar nodes, aortic nodes, sternal nodes drain lymph from thoracic organs and tissues
Popliteal nodes and Inguinal nodes drain lymph from lower limbs
Cistern chyli drain lymph from the abdominal and pelvic cavities

Lymphoid Tissue

This includes lymph glands called lymph nodes i.e. pharyngeal tonsils (adenoids) near the posterior nares, palatine tonsils at the back of the mouth and lingual tonsils at the back and sides of the tongue, aggregated lymphoid follicles (peyer’s patches) in the small intestines

Lymphoid tissue is found in the bone marrow, spleen, liver, lungs and thymus gland

Spleen

This is the largest lymph organ located in the left hypochondriac region of the abdominal cavity between fundus of the stomach and diaphragm

The spleen has two roles i.e.

site of old blood cell destruction
monitoring body immune system

The spleen filters blood

Bone Marrow

This acts as a site of

B-cell and T-cell generation.
It also produces monocyte, granulocytes, RBCs and platelets.

The B-cells mature in the bone marrow. The bone marrow is responsible for generating stem cells where all blood cells arise

Thymus Gland

This is a grayish organ located in the chest between lungs just below the neck

It has two lobes each with outer cortex and inner medulla. The medullar contains mature lymphocytes. The cortex receive pre-T cell

In cortex cell recognize certain antigen, those which fail die. The live cell continues to medulla and general circulation. This gland secrets thymosin required for development of T-lymphocytes

Function of lymph

Transport of proteins and large particles that cannot be absorbed directly into circulation.
Transport of fatty acids and cholesterol from intestines.
Return of excess fluid from tissues into circulation.
Carry bacteria into nearest lymph node where they can be destroyed.
Carry antibodies
Transport vitamin K from intestine to blood stream

Anatomy and Physiology of the Lymphatic System Read More »

Nephrotic and Nephritic syndromes

NEPHROTIC SYNDROME.

Nephrotic syndrome, or nephrosis, is a constellation of symptoms characterized by nephrotic range, massive proteinuria, edema, and hypoalbuminemia with or without hyperlipidemia.

MASSIVE Proteinuria >3.5g/24 hours Or spot urine protein: creatinine ratio >300 – 350 mg/mmol Hypoalbuminemia <25g/L,

Edema,(Generalized edema is called Anasarca)

And often: Hyperlipidemia/dyslipidemia (total cholesterol >10 mmol/L)

Additionally, the loss of immunoglobulins increases the risk of infection, while the loss of proteins that prevent clot formation puts patients at risk for blood clots.

Pathophysiology of Nephrotic Syndrome.

Nephrotic syndrome results from damage to the kidney’s glomeruli, the tiny blood vessels that filter waste and excess water from the blood and send them to the bladder as urine.

Damage to the glomeruli from diabetes or even prolonged hypertension causes the membrane to become porous, so that small proteins such as albumin pass through the kidneys into urine.

Glomerular Filtration Barrier Disruption: The renal glomerulus, responsible for filtering blood entering the kidney, consists of capillaries with small pores. In nephrotic syndrome, inflammation or hyalinization affects the glomeruli, allowing proteins, including albumin, antithrombin, and immunoglobulins, to pass through the normally restrictive cell membrane.
Proteinuria: Increased permeability results in the leakage of proteins into the urine. Albumin, a key protein for maintaining oncotic pressure in the blood, is lost in significant amounts.
Hypoalbuminemia: Loss of albumin in the urine reduces the oncotic pressure in the blood. Reduced oncotic pressure leads to the accumulation of fluid in the interstitial tissues, causing edema.
Hyperlipidemia: Hypoalbuminemia triggers compensatory mechanisms in the liver. The liver increases the synthesis of proteins such as alpha-2 macroglobulin and lipoproteins. Elevated lipoprotein levels contribute to hyperlipidemia associated with nephrotic syndrome.

Signs and symptoms

Manifestation of glomerular disease, characterized by nephrotic range proteinuria and a triad of clinical findings associated with large urinary losses of protein : hypoalbuminaemia , edema and hyperlipidemia

Weight Gain: Patients experience noticeable weight gain due to fluid retention. The retention of fluids, primarily as a result of massive proteinuria and reduced oncotic pressure, leads to increased body weight.

Facial Edema (Puffiness Around the Eyes): Swelling, particularly around the eyes, with a distinctive pattern. Generalized edema is called Anarsaca.

Morning Onset: The puffiness is most apparent in the morning and tends to subside throughout the day.
Location: Predominantly observed around the eyes.

Abdominal Swelling: Enlargement of the abdominal region. Associated with;

Pleural Effusion: Accumulation of fluid in the pleural cavity.
Labial or Scrotal Swelling: Swelling in the genital areas.

Edema of Intestinal Mucosa: Swelling of the intestinal mucosa leading to various gastrointestinal symptoms. Such as

Diarrhea: Resulting from edema affecting the intestinal lining.
Anorexia: Loss of appetite due to abdominal discomfort.
Poor Intestinal Absorption: Impaired absorption of nutrients, contributing to malnutrition.

Ankle/Leg Swelling: Edema affecting the lower extremities. Fluid accumulation in the ankles and legs due to altered fluid balance.

Behavioral Changes: Altered mood and behavior. Manifested as;

Irritability: Restlessness or frustration.
Easily Fatigued: Fatigue occurs more quickly than expected.
Lethargy: Persistent tiredness, indicating overall weakness.

Susceptibility to Infection: Increased vulnerability to infections. Loss of immunoglobulins in the urine, combined with potential immune system suppression from treatments like corticosteroids, increases the risk of infections.

Urine Alterations: Changes in urine characteristics. Such as;

Decreased Volume: Reduced urine output.
Frothy Urine: Presence of foam or bubbles in the urine, indicating significant proteinuria.
Lipiduria (lipids in urine) can also occur, but is not essential for the diagnosis of nephrotic syndrome. Hyponatremia also occurs with a low fractional sodium excretion.

Hyperlipidaemia: Hypoproteinemia stimulates protein synthesis in the liver, resulting in the overproduction of lipoproteins.

Anaemia (iron resistant microcytic hypochromic type) may be present due to transferrin loss.

Dyspnea may be present due to pleural effusion or due to diaphragmatic compression with ascites.

Other features: May have features of the underlying cause, such as the rash associated with systemic lupus erythematosus, or the neuropathy associated with diabetes.

Causes of Nephrotic Syndrome

Nephrotic syndrome has many causes and may either be the result of a glomerular disease that can be either limited to the kidney, called primary nephrotic syndrome (primary glomerulonephrosis), or a condition that affects the kidney and other parts of the body, called secondary nephrotic syndrome and other genetic causes.

Primary causes

Minimal change disease (MCD): is the most common cause of nephrotic syndrome in children. It owes its name to the fact that the nephrons appear normal when viewed with an optical microscope as the lesions are only visible using an electron microscope. Another symptom is a pronounced proteinuria.
Focal segmental glomerulosclerosis (FSGS): is the most common cause of nephrotic syndrome in adults. It is characterized by the appearance of tissue scarring in the glomeruli. The term focal is used as some of the glomeruli have scars, while others appear intact; the term segmental refers to the fact that only part of the glomerulus suffers the damage.
Membranous glomerulonephritis (MGN): The inflammation of the glomerular membrane causes increased leaking in the kidney. It is not clear why this condition develops in most people, although an auto-immune mechanism is suspected.
Membranoproliferative glomerulonephritis (MPGN): is the inflammation of the glomeruli along with the deposit of antibodies in their membranes, which makes filtration difficult.
Rapidly progressive glomerulonephritis (RPGN): (Usually presents as a nephritic syndrome) A patient’s glomeruli are present in a crescent moon shape. It is characterized clinically by a rapid decrease in the glomerular filtration rate (GFR) by at least 50% over a short period, usually from a few days to 3 months.

Secondary causes

Diabetic nephropathy: is a complication that occurs in some diabetics. Excess blood sugar accumulates in the kidney causing them to become inflamed and unable to carry out their normal function. This leads to the leakage of proteins into the urine.
Systemic lupus erythematosus: this autoimmune disease can affect a number of organs, among them the kidney, due to the deposit of immune complexes that are typical to this disease. The disease can also cause lupus nephritis.
Infections like; Syphilis: Kidney damage can occur during the secondary stage of this disease (between 2 and 8 weeks from onset). Hepatitis B: certain antigens present during hepatitis can accumulate in the kidneys and damage them. HIV: the virus’s antigens provoke an obstruction in the glomerular capillary’s lumen that alters normal kidney function.
Vasculitis: inflammation of the blood vessels at a glomerular level impedes the normal blood flow and damages the kidney.
Cancer: as happens in myeloma, the invasion of the glomeruli by cancerous cells disturbs their normal functioning.
Genetic disorders: congenital nephrotic syndrome is a rare genetic disorder in which the protein nephrin, a component of the glomerular filtration barrier, is altered.
Drugs ( e.g. gold salts, penicillin, captopril): gold salts can cause a more or less important loss of proteins in urine as a consequence of metal accumulation. Penicillin is nephrotoxic in patients with kidney failure and captopril can aggravate proteinuria.

Diagnosis and Investigations

Initial Assessment:

Obtain a thorough medical history, including any acute or chronic conditions, family history of kidney disease, and a review of systems to identify symptoms such as edema, fatigue, and foamy urine.
Perform a physical examination focusing on signs of fluid overload, such as edema and ascites, as well as other systemic findings.

Laboratory Investigations:

Conduct urinalysis to detect the features of nephrotic syndrome: high levels of proteinuria.
Microscopic hematuria that may occasionally be present.
Biochemical tests to evaluate kidney function, including serum creatinine, blood urea nitrogen (BUN), electrolytes, albumin levels, and a lipid profile, as hyperlipidemia is often associated with nephrotic syndrome.
Perform a urine protein-to-creatinine ratio to quantify the degree of proteinuria.

Imaging Studies:

Ultrasound imaging: the kidneys may appear hyperechoic with a loss of corticomedullary differentiation.
If indicated, conduct an ultrasound of the entire abdomen to evaluate for complications such as venous thrombosis or to rule out other causes of proteinuria.

Immunological and Serological Testing:

Analyze auto-immune markers, including antinuclear antibodies (ANA), anti-streptolysin O titers (ASOT), complement components (such as C3), cryoglobulins, and perform serum electrophoresis to detect monoclonal gammopathy.

Kidney Biopsy:

If the initial tests are inconclusive or if it is important to determine the specific cause of nephrotic syndrome, Carry out a kidney biopsy. Histological examination can identify the type of glomerulonephritis or other glomerular pathology.

Additional Investigations:

Consider genetic testing if there is a suspicion of hereditary causes of nephrotic syndrome, especially in pediatric cases or when there is a family history of kidney disease.
Assess for secondary causes of nephrotic syndrome, which may include tests for infectious diseases (like hepatitis B and C, HIV), diabetes mellitus control (HbA1c), and evaluation for malignancies if clinically indicated.

Treatment of Nephrotic Syndrome

Aims of Management.

To reduce edema
To correct hypoalbuminemia
To lower blood pressure
To reduce proteinuria
To prevent complications such as infection, thrombosis, and malnutrition

Medical Management:

Diuretics: Loop diuretics, such as furosemide, are the mainstay of treatment for edema. Thiazide diuretics, such as hydrochlorothiazide, can be added if needed.
Albumin: Albumin infusions may be necessary to correct hypoalbuminemia and reduce edema. Not used because they are expensive.
ACE inhibitors or ARBs: ACE inhibitors, such as lisinopril, or ARBs, such as losartan, are used to lower blood pressure and reduce proteinuria.
Corticosteroids: Prednisone is the most commonly used corticosteroid for the treatment of nephrotic syndrome. Prednisone is started at a dose of 1-2 mg/kg/day and then tapered over several weeks. Lack of response to prednisolone therapy for 4 weeks is an Indication for renal biopsy.
Immunosuppressive drugs: Immunosuppressive drugs, such as cyclophosphamide, are used to treat patients who do not respond to corticosteroids.
Statins: Statins, such as atorvastatin, are used to lower cholesterol levels.
Antiplatelet agents: Antiplatelet agents, such as aspirin, are used to prevent thrombosis.
Nutritional support: Nutritional support, including a high-protein diet, is important to prevent malnutrition.
Vitamin D and calcium supplements: Vitamin D and calcium supplements may be necessary to prevent hypocalcemia.
Antibiotics: Antibiotics are used to treat infections.
Vaccinations: Vaccinations against pneumococcal pneumonia and influenza are recommended for patients with nephrotic syndrome.

Nursing Interventions for Nephrotic Syndrome:

Fluid Volume Excess:

Elevate the child’s legs and feet to promote fluid drainage.
Monitor for signs of fluid overload, such as edema, ascites, and pleural effusions.
Restrict fluid intake as prescribed by the physician.
Administer diuretics, such as furosemide (Lasix), as prescribed to promote fluid excretion.
Monitor intake and output strictly and maintain accurate fluid balance charts.
Weigh the child daily to monitor fluid status.

Ineffective Breathing Pattern:

Assess respiratory status regularly, including oxygen saturation, respiratory rate, and effort.
Position the child in a semi-Fowler’s position or over a table supported by pillows to improve lung expansion.
Provide oxygen therapy, if prescribed, to maintain adequate oxygenation.
Encourage the child to take slow, deep breaths and use relaxation techniques to reduce anxiety and improve breathing patterns.
Administer bronchodilators, if prescribed, to improve airflow and reduce wheezing.

Risk for Infection:

Monitor the child for signs of infection, such as fever, chills, and increased white blood cell count.
Administer antibiotics, as prescribed, to treat or prevent infections.
Practice strict hand hygiene and maintain aseptic technique when handling the child and performing procedures.
Keep the child’s skin clean and dry to prevent skin infections.
Monitor the child’s nutritional status and provide a diet rich in protein and vitamins to support the immune system.

Altered Nutrition: Less Than Body Requirements:

Provide small, frequent meals that are high in protein and calories to meet the child’s increased nutritional needs.
Offer a variety of foods to encourage the child to eat and prevent monotony.
Consult with a registered dietitian to develop a personalized nutrition plan that meets the child’s individual needs and preferences.
Supplement the child’s diet with nutritional supplements, as prescribed, to ensure adequate intake of essential nutrients.

Dietary Management of Nephrotic Syndrome:

Provide a balanced diet with adequate protein (1.5-2 g/kg) and calories.
Limit fat intake to less than 30% of total calories and avoid saturated fats.
Encourage the child to follow a “no added salt” diet to reduce fluid retention.
Discourage the consumption of high-sugar drinks and snacks to prevent weight gain and fluid overload.
Monitor the child’s weight regularly and adjust the diet as needed to maintain a healthy weight.

Complications:

Monitor for complications of nephrotic syndrome, such as ascites, pleural effusion, generalized edema, coagulation disorders, thrombosis, recurrent infections, renal failure, growth retardation, and calcium and vitamin D deficiency.
Provide appropriate interventions and treatments for any complications that arise.
Educate the child and family about the potential complications of nephrotic syndrome and the importance of regular follow-up care.

Complications of Nephrotic Syndrome:

Thromboembolic Disorders: Caused by decreased levels of antithrombin III, a protein that inhibits blood clotting. Antithrombin III is lost in the urine due to the increased permeability of the glomerular basement membrane. This can lead to the formation of blood clots in the veins (deep vein thrombosis) or arteries (pulmonary embolism).
Infections: Increased susceptibility to infections due to:

Loss of immunoglobulins and other protective proteins in the urine.
Decreased production of white blood cells.
Impaired immune cell function.
Common infections include pneumonia, cellulitis, and peritonitis.

Acute Kidney Failure: Caused by a decrease in blood volume (hypovolemia) due to fluid loss into the tissues (edema). Hypovolemia leads to decreased blood flow to the kidneys, which can damage the kidneys and cause acute kidney failure.
Pulmonary Edema: Caused by the loss of proteins from the blood plasma, which leads to a decrease in oncotic pressure. Decreased oncotic pressure allows fluid to leak out of the blood vessels into the lungs, causing pulmonary edema.
Hypothyroidism: Caused by the loss of thyroxine-binding globulin (TBG), a protein that binds to thyroid hormone and transports it in the blood. Decreased TBG levels lead to decreased levels of free thyroid hormone, which can cause hypothyroidism.
Vitamin D Deficiency: Caused by the loss of vitamin D-binding protein, a protein that binds to vitamin D and transports it in the blood. Decreased vitamin D-binding protein levels lead to decreased levels of free vitamin D, which can cause vitamin D deficiency.
Hypocalcemia: Caused by the loss of 25-hydroxycholecalciferol, the storage form of vitamin D. Vitamin D is necessary for the absorption of calcium from the intestines. Decreased vitamin D levels lead to decreased calcium absorption, which can cause hypocalcemia.
Microcytic Hypochromic Anemia: Caused by the loss of ferritin, a protein that stores iron in the body. Decreased ferritin levels lead to decreased iron stores, which can cause iron-deficiency anemia.
Protein Malnutrition: Caused by the loss of protein in the urine, which exceeds the amount of protein that is ingested. Protein malnutrition can lead to a number of health problems, including weakness, fatigue, and impaired immune function.
Growth Retardation: Can occur in children with nephrotic syndrome due to a number of factors, including:

Protein malnutrition.
Anorexia (reduced appetite).
Steroid therapy (which can suppress growth).

Cushing’s Syndrome: Can occur in patients with nephrotic syndrome who are treated with high doses of corticosteroids. Cushing’s syndrome is caused by the overproduction of the hormone cortisol, which can lead to a number of health problems, including weight gain, high blood pressure, and diabetes.

NEPHRITIC SYNDROME

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Differences between Nephrotic syndrome and Nephritic syndrome

Nephrotic and Nephritic syndromes Read More »

Glomerulonephritis

Glomerulonephritis (GN)

Glomerulonephritis (GN) refers to a group of kidney diseases characterized primarily by inflammation and damage to the glomeruli, the tiny filtering units within the kidneys.

Glomerulonephritis is an inflammatory condition of the kidneys characterized by increased permeability of the glomerular filtration barrier causing filtration of RBCs and proteins.

While the primary site of injury is the glomerulus, inflammation can sometimes extend to the small blood vessels (capillaries, arterioles) within the kidney.

Bilateral Involvement: GN usually affects both kidneys simultaneously due to the systemic nature of many underlying causes (e.g., immune responses, infections).

Review of Relevant Anatomy and Physiology: The Nephron and Glomerulus

Functional Unit: The nephron is the fundamental structural and functional unit of the kidney, responsible for filtering blood and producing urine. Each kidney contains approximately 1 million nephrons.

Nephron Structure:

Glomerular Capsule (Bowman’s Capsule): A cup-shaped structure at the closed end of the nephron tubule. It surrounds the glomerulus.
Glomerulus: A network (tuft) of tiny arterial capillaries enclosed within Bowman’s capsule. This is where blood filtration begins. Blood enters via the afferent arteriole and exits via the efferent arteriole.
Renal Tubule: Extending from Bowman’s capsule, this tubule is about 3 cm long and consists of three main parts:

Proximal Convoluted Tubule (PCT): Responsible for reabsorbing the majority of filtered water, electrolytes (Na+, K+, Cl-), glucose, amino acids, and bicarbonate.
Loop of Henle: A hairpin-shaped loop (with descending and ascending limbs) extending into the medulla. Crucial for establishing the concentration gradient in the kidney, allowing for urine concentration. Further water and electrolyte reabsorption occurs here.
Distal Convoluted Tubule (DCT): Involved in fine-tuning electrolyte and acid-base balance (e.g., reabsorbing Na+, Ca++; secreting K+, H+). Influenced by hormones like aldosterone and ADH (indirectly).

Collecting Duct: Several DCTs empty into a collecting duct. These ducts pass through the medulla, further adjusting water reabsorption (under ADH influence) and electrolyte balance before delivering urine to the renal pelvis.

Glomerular Filtration Membrane (GFM): The crucial barrier separating blood in the glomerular capillaries from the filtrate in Bowman’s space. It consists of three layers:

Endothelium: The inner lining of the capillaries, featuring fenestrations (pores) that allow passage of water and small solutes but block blood cells.
Glomerular Basement Membrane (GBM): A middle layer, acting as a key size-selective and charge-selective barrier, preventing larger proteins (like albumin) from passing through.
Epithelial Cells (Podocytes): The outer layer facing Bowman’s space. These cells have foot processes (pedicels) separated by filtration slits, covered by a slit diaphragm, providing a final barrier, particularly to medium-sized proteins.

Glomerular Filtration Rate (GFR): The volume of fluid filtered from the glomerular capillaries into Bowman’s capsule per unit of time.

Normal GFR: Approximately 125 mL/minute or 180 Liters/day.
Filtration Process: Water and small molecules (electrolytes, glucose, urea, amino acids) pass freely through the GFM. Blood cells and large proteins (like albumin) are normally retained in the blood.
Reabsorption: Most of the filtrate (over 99%) is reabsorbed back into the bloodstream by the renal tubules. Only about 1-1.5 mL of fluid per minute is typically excreted as urine.

Renal Blood Flow Regulation: The kidneys have intrinsic mechanisms (autoregulation) and are influenced by the autonomic nervous system (sympathetic and parasympathetic nerves) and hormones (like angiotensin II, prostaglandins) to maintain relatively stable blood flow and GFR despite fluctuations in systemic blood pressure.

Classification of Glomerulonephritis

GN can be classified in several ways, which often overlap:

Onset and Duration:

Acute Glomerulonephritis (AGN): Develops suddenly, often following an infection (like streptococcus). Onset can be days to weeks after the trigger. Typically presents with nephritic features (see below).
Chronic Glomerulonephritis (CGN): Develops gradually over several years, often silently in the early stages. It may follow an episode of acute GN or arise insidiously. It represents progressive scarring and loss of kidney function, eventually leading to Chronic Kidney Disease (CKD).
Rapidly Progressive Glomerulonephritis (RPGN): Characterized by rapid loss of kidney function (often a 50% decline in GFR within weeks to months). Histologically associated with crescent formation in Bowman’s space. This is a medical emergency.

Histological Pattern (Based on Kidney Biopsy):

Proliferative GN: Characterized by an increase in the number of cells within the glomerulus (e.g., endothelial, mesangial, epithelial cells, infiltrating inflammatory cells). Examples include:

IgA Nephropathy (most common primary GN worldwide)
Post-Infectious GN (e.g., post-streptococcal)
Membranoproliferative GN (MPGN)
Lupus Nephritis (certain classes)
RPGN (Crescentic GN)

Non-Proliferative GN: Characterized primarily by structural changes without significant hypercellularity. Examples include:

Minimal Change Disease (common cause of nephrotic syndrome in children)
Focal Segmental Glomerulosclerosis (FSGS)
Membranous Nephropathy (common cause of nephrotic syndrome in adults)

Clinical Manifestations (Signs and Symptoms)

Symptoms vary widely depending on the type, severity, and acuity of GN. Some patients may be asymptomatic initially.

Common Features (especially Nephritic pattern):

Hematuria: Blood in the urine. May be microscopic (detected only by test) or macroscopic (visible, often described as cola-colored, tea-colored, or smoky). RBC casts in urine sediment are highly suggestive of glomerular origin.
Proteinuria: Excess protein in the urine. Can range from mild to nephrotic range (>3.5g/day). May cause foamy urine.
Edema: Swelling, often starting around the eyes (periorbital edema, especially in the morning) and progressing to the legs (pedal edema), ankles, and potentially generalized (anasarca), including ascites (fluid in abdomen) and pleural effusions (fluid around lungs). Due to sodium/water retention and sometimes low albumin (in nephrotic syndrome).
Hypertension: New onset or worsening high blood pressure. Often related to fluid retention. Can be severe.
Oliguria/Anuria: Decreased urine output (<400-500 mL/day) or very low/no urine output. Indicates significant decline in GFR.
Dysuria: Painful urination (less common, but can occur).

Systemic Symptoms:

Fatigue/Malaise/Weakness: Due to anemia (from reduced erythropoietin production by failing kidneys or chronic inflammation), uremia, or the underlying disease.
Flank Pain: Aching pain in the back/sides over the kidney area (less common than in kidney stones or pyelonephritis, but can occur due to capsular stretching).
Fever & Chills: More common in acute, infection-related GN or systemic inflammatory conditions.
Headache: Often related to hypertension.
Gastrointestinal Disturbances: Nausea, vomiting, anorexia, abdominal pain (can be due to uremia or ascites).

Symptoms Related to Complications or Underlying Disease:

Shortness of Breath: Due to pulmonary edema (fluid in lungs) from fluid overload or heart failure.
Visual Disturbances: Blurred vision due to hypertensive retinopathy or retinal edema.
Symptoms of SLE, Vasculitis, etc.: Rash, joint pain, etc.
Chronic GN Symptoms: May be subtle initially, presenting later with signs of CKD like nocturia (frequent urination at night), bone pain/deformity (renal osteodystrophy), anemia, failure to thrive (in children).

Clinical Presentation of Glomerulonephritis

Nephritic Syndrome: Characterized by inflammation.

Key features include Hematuria (blood in urine, often cola-colored),
Hypertension,
Oliguria (reduced urine output),
Azotemia (increased BUN/Creatinine), and
mild to moderate Proteinuria.
Edema is common.
Post-streptococcal GN is a classic example.

Nephrotic Syndrome: Characterized by

heavy proteinuria (>3.5 g/day ),
Hypoalbuminemia (low blood albumin),
severe Edema, and
Hyperlipidemia (high cholesterol/triglycerides).
Minimal Change Disease and Membranous Nephropathy are classic examples.
(Note: Some GN types can present with mixed nephritic/nephrotic features or evolve from one pattern to another).

Etiology of Glomerulonephritis

Primary GN: The disease originates within the kidney itself, without evidence of a systemic disease trigger (though often immune-mediated). Examples: IgA Nephropathy, Minimal Change Disease, FSGS, Membranous Nephropathy.
Secondary GN: Occurs as a consequence of another underlying systemic disease or condition. Examples: Lupus Nephritis (from SLE), Diabetic Nephropathy, Vasculitis-associated GN (e.g., Wegener’s/GPA, Microscopic Polyangiitis), Anti-GBM Disease (Goodpasture’s Syndrome), GN related to infections (Hepatitis B/C, HIV, Endocarditis), certain cancers, or drug reactions.

Factors that can cause or increase the risk of developing GN include:

Infections:

Streptococcal Infections: Group A beta-hemolytic streptococci (causing strep throat or skin infections like impetigo) are a classic trigger for Post-Streptococcal Glomerulonephritis (PSGN), especially in children. Typically occurs 1-3 weeks after infection.
Other Bacterial Infections: Bacterial endocarditis, infected shunts.
Viral Infections: Hepatitis B, Hepatitis C, HIV.
Fungal/Parasitic Infections: Less common causes.

Immune Diseases (Autoimmune Conditions):

Systemic Lupus Erythematosus (SLE): Lupus nephritis is a common and serious complication.
Goodpasture’s Syndrome: Autoantibodies attack the GBM in kidneys and lungs.
IgA Nephropathy (Berger’s Disease): IgA antibody deposits in the glomeruli.
Vasculitis: Inflammation of blood vessels (e.g., Granulomatosis with Polyangiitis [Wegener’s], Microscopic Polyangiitis, Henoch-Schönlein Purpura [IgA Vasculitis]).

Systemic Diseases:

Diabetes Mellitus: Diabetic nephropathy is a leading cause of CKD, involving glomerular damage.
Hypertension: Can both cause kidney damage (nephrosclerosis) and be a consequence of GN. High BP exacerbates glomerular injury.

Hereditary Factors: Some forms of GN, like Alport syndrome or certain types of FSGS, have a genetic basis.

Other Factors:

Certain Cancers (e.g., lymphomas, solid tumors via paraneoplastic syndromes).
Exposure to certain drugs or toxins (e.g., NSAIDs, lithium, some antibiotics).
Idiopathic: In many cases, the specific cause remains unknown.

Pathophysiology of Glomerulonephritis

Acute glomerulonephritis following an infection and is thought to be as a result of immunological response.
The body responds to streptococci by producing antibodies which combine with bacterial antigens to form immune complexes.
As these antigen-antibody complexes travel through circulation, they get trapped in the glomeruli and activate an inflammatory response that results in injury to capillary walls.
As a result of the inflammation, the capillary lumen becomes smaller leading to renal insufficiency .
Injury to the capillaries increases permeability to large molecules-proteins hence can leak into urine.

Structural Damage:

Thickening of GFM: Basement membrane can thicken due to deposits or increased matrix production.
Cell Proliferation: Increased cell numbers within the glomerulus.
Podocyte Injury: Damage or effacement (flattening) of podocyte foot processes leads to increased protein leakage (proteinuria).
Breaks in GFM: Allows passage of red blood cells (hematuria) and larger amounts of protein.
Crescent Formation (in RPGN): Proliferation of cells (parietal epithelial cells, infiltrating macrophages) in Bowman’s space, compressing the glomerular tuft.

Functional Consequences:

Decreased GFR: Inflammation, scarring, and reduced filtration surface area impair the kidney’s ability to filter waste products.
Increased Permeability: Damage to the GFM leads to proteinuria and hematuria.

Progression:

Scarring (Glomerulosclerosis): Persistent injury leads to replacement of functional glomerular tissue with scar tissue.
Tubulointerstitial Fibrosis: Damage often extends to the surrounding tubules and interstitial tissue.
Loss of Nephrons: Progressive scarring leads to irreversible loss of nephrons and decline in kidney function (CKD).

Consequences of Reduced GFR and Damage:

Retention of Sodium and Water: Impaired filtration leads to fluid overload.
Hypertension: Caused by fluid overload and activation of the Renin-Angiotensin-Aldosterone System (RAAS).
Edema: Accumulation of excess fluid in interstitial spaces.
Azotemia/Uremia: Accumulation of nitrogenous waste products (urea, creatinine) in the blood.

Types of Glomerulonephritis

1. Diffuse proliferative glomerulonephritis

This is inflammation of the glomerulus affecting all glomeruli (diffuse) with an increased number of cells in them (proliferative). It usually follows transient infection especially beta hemolytic streptococci but other organisms can cause it.

It presents as acute nephritis with haematuria and proteinuria. Recovery is good in children and in adults 40% cases may develop hypertension and renal failure.

2. Focal/segmental proliferative glomerulonephritis:

This is inflammation of the glomerulus affecting some glomeruli (focal) with increased number of cells in them (proliferative). It is associated with systemic lupus erythematosus(SLE) or infective endocarditis. It presents also as an acute nephritis with haematuria and proteinuria and recovery is variable.

3. Membranous/mesangial proliferative/ membranoproliferative glomerulonephritis.

This is inflammation of the glomerulus with thickening of the glomerular basement membrane. It is due to infections like syphilis, malaria, hepatitis B, drugs like penicillamine, gold, diamorphine and tumors.

It presents as nephrotic syndrome with haematuria and proteinuria and recovery is variable but most case progress to chronic renal failure

4. Minimal change glomerulonephritis

This is inflammation of the glomerulus with no exact known cause. It presents as nephrotic syndrome with haematuria and proteinuria and recovery is good in children but recurrences are common in adults.

Glomerulonephritis can be acute if it occurs in days or weeks ie 1 – 3 weeks following a streptococcal infection or glomerular damage
Chronic glomerulonephritis occur over months or years and is characterized by progressive destruction (sclerosis) or glomeruli and gradual loss of renal function

Diagnostic Evaluation of Glomerulonephritis

A combination of history, physical exam, and laboratory/imaging tests are used. Kidney biopsy is often the definitive test.

History:

Recent infections (sore throat, skin infection).
Symptoms: onset, duration, nature (edema, urine color changes, fatigue, HTN).
Past medical history (diabetes, SLE, hypertension, prior kidney disease).
Family history of kidney disease.
Medication history (including NSAIDs, nephrotoxic drugs).

Physical Examination:

Blood pressure measurement.
Assessment for edema (periorbital, peripheral, ascites).
Signs of fluid overload (jugular venous distension, lung crackles/rales indicating pulmonary edema).
Skin examination (rashes, signs of infection like impetigo, signs of vasculitis).
Observation for pallor (anemia), signs of uremia (e.g., uremic frost – rare now).
Assessment of visual acuity and fundoscopy (for hypertensive changes).

Urinalysis (Crucial first step):

Dipstick: Detects protein, blood, leukocytes, nitrites.
Microscopy: Quantifies RBCs, WBCs. Crucially looks for casts (cylindrical structures formed in tubules):

RBC Casts: Strongly suggest glomerular bleeding (hallmark of nephritic syndrome).
WBC Casts: Indicate inflammation (can be seen in GN, pyelonephritis, interstitial nephritis).
Granular Casts/Waxy Casts: Indicate tubular damage/stasis, often seen in more chronic disease.

Urine Protein Quantification: 24-hour urine collection or spot urine protein-to-creatinine ratio (UPCR) or albumin-to-creatinine ratio (UACR) to measure protein loss accurately.
Urine pH, specific gravity.

Blood Tests:

Renal Function Tests: Blood Urea Nitrogen (BUN) and Serum Creatinine (elevated levels indicate reduced GFR). Estimated GFR (eGFR) calculation.
Electrolytes: Sodium, Potassium (can be elevated, especially with oliguria), Chloride, Bicarbonate (may be low – metabolic acidosis). Calcium, Phosphorus (abnormalities common in CKD).
Complete Blood Count (CBC): Assess for anemia (normocytic, normochromic often seen in CKD), signs of infection.
Serum Albumin: Low levels (hypoalbuminemia) are characteristic of nephrotic syndrome.
Lipid Profile: Cholesterol and triglycerides are often elevated in nephrotic syndrome.
Inflammatory Markers: Erythrocyte Sedimentation Rate (ESR) or C-Reactive Protein (CRP) may be elevated.
Serological Tests (to identify cause):

Complement Levels (C3, C4): Low C3 is typical in post-streptococcal GN and some forms of MPGN/lupus nephritis. C4 may also be low in lupus.
Anti-Streptolysin O (ASO) Titre: Elevated titres suggest recent streptococcal infection (useful for PSGN diagnosis). Anti-DNase B is another marker for strep.
Antinuclear Antibody (ANA): Screening test for SLE.
Anti-dsDNA Antibody: Specific for SLE.
Anti-Glomerular Basement Membrane (Anti-GBM) Antibody: For Goodpasture’s syndrome.
Antineutrophil Cytoplasmic Antibodies (ANCA – c-ANCA, p-ANCA): For ANCA-associated vasculitis (GPA, MPA).
Hepatitis B/C Serology, HIV Test: To rule out infection-associated GN.

Imaging Studies:

Renal Ultrasound (USG): Assesses kidney size (often normal/enlarged in acute GN, small/scarred in chronic GN), echogenicity, rules out obstruction, and guides biopsy.
Chest X-ray: May show signs of fluid overload (pulmonary edema, pleural effusions, cardiomegaly).
Intravenous Pyelogram (IVP): Less commonly used now due to contrast risks and availability of other imaging; previously used to visualize urinary tract structures. CT or MRI may sometimes be used.

Kidney Biopsy:

Gold Standard: Provides a definitive diagnosis by allowing histological examination of kidney tissue (glomeruli, tubules, interstitium, vessels).
Information Gained: Identifies the specific type of GN, assesses the severity of inflammation/scarring (activity and chronicity), guides treatment decisions, and helps determine prognosis. Performed using light microscopy, immunofluorescence (to detect immune deposits like IgG, IgA, IgM, C3, C1q), and electron microscopy (for ultrastructural details like deposit location, podocyte changes).

Management of Glomerulonephritis

Aims of Management

Treatment goals depend on the type, severity, and underlying cause of GN.

General goals include:

preserving kidney function,
managing symptoms,
treating the underlying cause if possible, and
preventing complications.

General Supportive Measures:

Blood Pressure Control: Crucial for slowing progression. Often requires multiple medications. ACE inhibitors (ACEi) or Angiotensin II Receptor Blockers (ARBs) are often preferred as they can also reduce proteinuria. Target BP is usually <130/80 mmHg, potentially lower if proteinuria is significant.

Maintain Healthy Weight: Through appropriate diet and exercise (as tolerated).

Fluid Management:

Sodium and Water Restriction: To control edema and hypertension. Fluid intake may be limited based on urine output and fluid status.
Diuretics: Loop diuretics (e.g., furosemide) are commonly used to manage fluid overload and edema. Thiazides may be added if needed.

Dietary Modifications:

Protein Restriction: May be recommended in CKD to reduce workload on kidneys, but needs careful balancing to avoid malnutrition. Limit usually guided by GFR level. Less restriction or even normal intake may be needed in nephrotic syndrome to compensate for losses, requires careful monitoring.
Potassium, Phosphorus, Magnesium Restriction: Necessary if levels are elevated, common in advanced CKD. Requires avoiding certain foods and potentially using phosphate binders.
Calcium Supplements: May be needed if dietary intake is low or due to CKD mineral bone disease, often alongside Vitamin D analogues.

Specific Treatments (Based on GN type/cause):

Treating Underlying Infections: Antibiotics for bacterial infections (e.g., penicillin for post-streptococcal GN prevention in outbreaks or treating active infection; treatment for endocarditis). Antivirals for Hepatitis B/C or HIV.

Plasma Exchange (Plasmapheresis): Removes harmful antibodies from the blood. Used in conditions like Anti-GBM disease and severe ANCA-associated vasculitis.

Immunosuppression: Used for many primary immune-mediated GN and secondary forms like lupus nephritis or vasculitis. Aims to reduce inflammation and harmful immune responses.

Corticosteroids (e.g., Prednisone): Mainstay for many types.
Cytotoxic Agents (e.g., Cyclophosphamide, Mycophenolate Mofetil [MMF], Azathioprine): Used for more severe or resistant cases.
Calcineurin Inhibitors (e.g., Tacrolimus, Cyclosporine): Used for some types like Minimal Change, FSGS, Membranous.
Biologic Agents (e.g., Rituximab – targets B cells): Increasingly used for ANCA vasculitis, lupus nephritis, some other types.
(Immunosuppression carries risks of infection, malignancy, and other side effects, requiring careful monitoring).

Management of Complications:

Dialysis (Hemodialysis or Peritoneal Dialysis): Required for acute kidney injury with severe complications (fluid overload, hyperkalemia, acidosis, uremia) or for End-Stage Renal Disease (ESRD) when GFR is very low (<15 mL/min).
Anemia Management: Erythropoiesis-stimulating agents (ESAs) and iron supplementation.
Mineral and Bone Disorder Management: Phosphate binders, Vitamin D analogues, calcimimetics.
Hyperlipidemia Management: Statins may be used, especially in nephrotic syndrome.

Lifestyle Changes & Patient Education:

Adherence to medications, diet, and fluid restrictions.
Regular monitoring of BP, weight, and symptoms.
Smoking cessation.
Avoidance of nephrotoxic substances (e.g., NSAIDs, certain contrast dyes).
Understanding the disease, treatment plan, and potential complications.

Physiotherapy and Supportive Care:

Endurance Exercise: As tolerated (walking, swimming, cycling) can improve cardiovascular health, circulation, and well-being. Helps kidneys discharge waste and toxins by improving overall circulation.
Breathing Exercises: Pursed-lip breathing and diaphragmatic breathing can help manage shortness of breath associated with fluid overload or anxiety.
Edema Management: Elevation of edematous limbs, gentle range-of-motion exercises. Lymphatic massage may be considered for persistent edema, but primary treatment is addressing the underlying fluid overload medically.
Energy Conservation Techniques: Pacing activities, rest periods, especially if fatigued due to anemia or uremia.

Nursing Management

Goals of Nursing Care:

Maintain fluid and electrolyte balance.
Achieve and maintain target blood pressure.
Alleviate pain and discomfort.
Maintain effective breathing pattern and gas exchange.
Prevent skin breakdown.
Prevent infection.
Maintain adequate nutritional status.
Patient verbalizes understanding of disease and treatment plan.
Patient copes effectively with diagnosis and lifestyle changes.

Assessment:

Vital Signs: Frequent BP monitoring, heart rate, respiratory rate, temperature.
Fluid Balance: Strict intake and output monitoring, daily weights (most sensitive indicator of fluid status), assessment for edema (location, severity, pitting), jugular venous distension, lung sounds.
Symptoms: Assess for changes in urine (color, amount, foaminess), fatigue, shortness of breath, pain, nausea/vomiting.
Skin Integrity: Assess edematous areas for breakdown.
Neurological Status: Assess for headache, visual changes, confusion (signs of severe HTN or uremia).
Psychosocial Assessment: Coping mechanisms, anxiety, knowledge about the disease.
Monitor Lab Results: BUN, Creatinine, electrolytes, CBC, albumin, etc.

Nursing Diagnoses :

Excess Fluid Volume related to compromised regulatory mechanisms (renal failure) and sodium/water retention as evidenced by edema, weight gain, hypertension, abnormal lung sounds, decreased urine output.
Acute Pain related to inflammation of the renal cortex/capsular distension as evidenced by patient report of flank pain, facial grimacing.
Ineffective Breathing Pattern or Impaired Gas Exchange related to fluid overload (pulmonary edema) as evidenced by dyspnea, tachypnea, abnormal breath sounds, low oxygen saturation.
Risk for Impaired Skin Integrity related to edema.
Decreased Activity tolerance related to fatigue (anemia, uremia) and fluid overload.
Inadequate nutritional intake related to anorexia, nausea, dietary restrictions.
Risk for Infection related to altered immune status or immunosuppressive therapy.
Disrupted Body Image related to edema, presence of dialysis access, or chronic illness.
Excessive anxiety related to diagnosis, prognosis, and treatment complexity.
Deficient Knowledge related to disease process, dietary restrictions, medications, and self-care management.

Interventions:

Fluid Management: Administer diuretics as ordered, enforce fluid/sodium restrictions accurately, monitor I&O and daily weights meticulously, elevate edematous extremities, assist with frequent position changes to mobilize fluid and prevent skin breakdown.
Blood Pressure Management: Administer antihypertensives as ordered, monitor BP closely (before/after meds, postural checks if indicated).
Pain Management: Assess pain thoroughly (onset, location, quality, severity), provide comfort measures (positioning, quiet environment), administer analgesics as ordered (use caution with NSAIDs), explore relaxation techniques/diversion therapy.
Respiratory Support: Elevate head of bed (Semi-Fowler’s or High-Fowler’s position) to ease breathing, monitor respiratory status (rate, depth, effort, O2 saturation), administer oxygen as needed, encourage deep breathing/coughing exercises (if appropriate, not overly strenuous).
Nutritional Support: Collaborate with dietitian, provide prescribed diet, monitor intake, manage nausea/vomiting (antiemetics as ordered), provide oral care.
Skin Care: Gentle cleansing, moisturizing, use pressure-relieving surfaces if bed-bound, handle edematous skin carefully.
Activity Management: Encourage rest periods, assist with ADLs as needed, gradually increase activity as tolerated, plan activities to conserve energy.
Infection Prevention: Monitor for signs of infection (fever, increased WBC, site-specific signs), use aseptic technique, educate patient on hand hygiene and avoiding sick contacts (especially if immunosuppressed).
Medication Administration: Administer all medications accurately and on time (diuretics, antihypertensives, immunosuppressants, antibiotics, phosphate binders, etc.), monitor for therapeutic effects and side effects. Administer albumin infusions as ordered (helps shift fluid from interstitial space to intravascular space, often followed by diuretics).
Psychosocial Support: Provide emotional support, encourage verbalization of feelings, involve family, provide clear explanations, refer to support groups or counseling if needed.
Patient Education: Teach about the disease, medications (purpose, dose, side effects), dietary/fluid restrictions, monitoring (BP, weight, symptoms), when to seek medical attention, importance of follow-up.
Preparation for Procedures: Educate and prepare patient for kidney biopsy, dialysis initiation if necessary.

Complications of Glomerulonephritis

GN can lead to various acute and chronic complications:

Acute Kidney Injury (AKI) / Acute Renal Failure: Rapid decline in kidney function.
Chronic Kidney Disease (CKD): Progressive, irreversible loss of kidney function over time.
End-Stage Renal Disease (ESRD): Kidney function fails completely, requiring dialysis or transplantation.
Nephrotic Syndrome: (If not the primary presentation).
Hypertension: Often difficult to control, increases cardiovascular risk.
Electrolyte Imbalances: Hyperkalemia (high potassium – dangerous!), hyperphosphatemia, hypocalcemia, metabolic acidosis.
Anemia: Due to decreased erythropoietin production.
Increased Susceptibility to Infections: Due to the disease itself or immunosuppressive therapy.
Cardiovascular Disease: Increased risk of heart attack, stroke.
Renal Osteodystrophy: Bone disease related to CKD.
Hypertensive Encephalopathy: Neurological symptoms due to severely elevated blood pressure (headache, confusion, seizures).
Fluid Overload: Leading to:

Pulmonary Edema: Fluid accumulation in the lungs, causing severe shortness of breath.
Congestive Heart Failure (CHF): Heart struggles to cope with excess fluid volume.

Glomerulonephritis Read More »

Renal Failure

RENAL FAILURE (Acute and Chronic)

Renal failure refers to reduction in renal/kidney function.

Renal failure, also known as kidney failure, describes a situation where the kidneys lose their ability to function adequately.

This means they cannot effectively filter waste products from the blood, regulate electrolytes and fluids, or perform their essential endocrine functions.

The term “renal insufficiency” was formerly used but “kidney failure” is now more common, especially when function is significantly impaired.

The fundamental issue in renal failure is a reduction in the kidney’s excretory and regulatory functions.

Excretory Function Loss: Inability to remove metabolic wastes (like urea, creatinine, uric acid) and excess electrolytes (like potassium, phosphate) from the blood and excrete them in urine.

Regulatory Function Loss: Impaired ability to maintain:

Fluid balance (leading to overload or dehydration).
Electrolyte balance (e.g., potassium, sodium, calcium, phosphate).
Acid-base balance (often leading to metabolic acidosis).
Blood pressure control (through renin-angiotensin system and fluid balance).

Consequences of Kidney Function Failure:

Waste Product Accumulation: Toxic metabolic byproducts (urea, creatinine, nitrogenous wastes) build up in the blood – a condition known as azotemia. If symptoms develop due to azotemia, it’s called uremia.

Fluid Imbalance: Kidneys struggle to excrete excess fluid, leading to fluid overload, edema (swelling in legs, ankles, feet, lungs), and hypertension.

Electrolyte Disturbances:

Hyperkalemia: High potassium levels (critical, can cause fatal heart rhythm problems).
Hyperphosphatemia/Hypocalcemia: High phosphate and low calcium (due to decreased excretion of phosphate and impaired Vitamin D activation). This leads to bone disease.
Sodium Imbalance: Can be high, low, or normal depending on fluid status and intake/output.

Acid-Base Disturbances: Kidneys cannot excrete metabolic acids or regenerate bicarbonate effectively, leading to metabolic acidosis.

Endocrine Disruption:

Decreased production of erythropoietin (EPO), leading to anemia.
Impaired activation of Vitamin D, contributing to hypocalcemia and bone disease (renal osteodystrophy).
Altered insulin metabolism (kidneys help degrade insulin; failure can lead to longer insulin half-life).

Types of Renal Failure:

Acute Renal Failure (ARF) / Acute Kidney Injury (AKI): Characterized by a sudden onset (hours to days) of kidney dysfunction, often reversible if the underlying cause is treated promptly.
Chronic Renal Failure (CRF) / Chronic Kidney Disease (CKD): Characterized by a gradual, progressive, and irreversible loss of kidney function occurring over months to years.

ACUTE RENAL FAILURE (ARF) / ACUTE KIDNEY INJURY (AKI)

Acute Renal Failure is the rapid decline in the kidney’s ability to clear the blood of toxic substances e.g poison, drugs and antibodies that react against the kidneys leading to accumulation of metabolic waste products e.g. urea in blood.

AKI is the abrupt loss of kidney function, resulting in the retention of urea and other nitrogenous waste products and the dysregulation of extracellular volume and electrolytes. It’s characterized by a sudden and often complete loss of the kidneys’ ability to remove waste, occurring over hours, days, or sometimes weeks. While potentially reversible, it carries significant morbidity and mortality.

A healthy adult eating a normal diet needs a minimum daily urine output of approximately 400 ml to excrete the body’s waste products through the kidneys. An amount lower than this indicates a decreased GFR.

Key Markers/Characteristics: AKI is usually marked by:

Decreased Glomerular Filtration Rate (GFR): A rapid decline in the rate at which the kidneys filter blood.
Increased Serum Creatinine and BUN: Azotemia develops quickly as waste products accumulate. Creatinine rise is a key diagnostic indicator.
Oliguria: Urine output less than 400 ml per day (or <0.5 ml/kg/hr). However, AKI can also be non-oliguric, where urine output is normal or even high, but the kidneys are still not filtering waste effectively. Anuria (urine output <100 ml/day) can also occur.
Hyperkalemia: Potentially life-threatening elevation of potassium levels due to impaired excretion. (Normal K+ range approx. 3.6 to 5.2 mmol/L).
Sodium and Water Retention: Leading to edema and hypertension.
Metabolic Acidosis: Due to impaired acid excretion.

Risk Factors for AKI:

Hospitalization: Especially ICU admission.
Advanced Age: Reduced baseline GFR, more comorbidities.
Pre-existing Chronic Kidney Disease (CKD): Reduced renal reserve.
Diabetes Mellitus: Underlying nephropathy, vascular disease.
Hypertension: Underlying vascular disease.
Heart Failure: Reduced cardiac output, cardiorenal syndrome.
Liver Disease: Hepatorenal syndrome, altered hemodynamics.
Peripheral Artery Disease: Marker of systemic atherosclerosis, may involve renal arteries.
Sepsis: Hypotension, inflammation, direct kidney effects.
Volume Depletion (Dehydration): Common precipitant.
Exposure to Nephrotoxins: Contrast dye, certain antibiotics (aminoglycosides, vancomycin), NSAIDs.
Major Surgery: Especially cardiac or vascular surgery (risk of hypotension, emboli).

Pathophysiology of Acute Renal Failure/Acute Kidney Failure

Although the pathogenesis of Acute Renal Failure and oliguria is not always known, many times there is a specific underlying problem.

There are underlying problems that cause the development of Acute Renal Failure such as hypovolemia, hypotension, reduced cardiac output and failure, and obstruction of the kidney.

Pathophysiology Summary (Simplified Flow):
Initial Insult (Prerenal, Intrarenal, Postrenal) → Decreased Renal Perfusion / Direct Tubular/Glomerular Damage / Obstruction → Decreased GFR → Activation of RAAS & Sympathetic Nervous System (attempt to preserve BP/volume) → Renal Vasoconstriction → Further Decrease in Renal Blood Flow & GFR → Tubular Cell Injury/Dysfunction (impaired reabsorption/secretion) → Sodium & Fluid Retention (Edema, Hypertension) → Decreased Waste Excretion (Azotemia) → Decreased Acid Excretion (Metabolic Acidosis) → Decreased Potassium Excretion (Hyperkalemia) → Oliguria / AKI Manifestations

Etiology of Acute Renal Failure

A. Prerenal Acute Renal Failure:

This category involves conditions that reduce blood supply to the kidneys, leading to ischemia (reduced blood flow) and damage to the kidney tissue. The kidneys are highly sensitive to blood flow reduction, as they require a constant supply of oxygen and nutrients to function properly.

1. Hypovolemia (Low Blood Volume):

Causes:

Hemorrhage: Significant blood loss due to trauma, surgery, or internal bleeding.
Anemia: Severe anemia reduces the oxygen-carrying capacity of the blood, leading to insufficient oxygen delivery to the kidneys.
Asphyxia: Suffocation or airway obstruction reduces oxygen intake, compromising oxygen supply to the kidneys.
Burns: Extensive burns lead to fluid loss and decreased blood volume.
Dehydration: Inadequate fluid intake or excessive fluid loss due to sweating, vomiting, or diarrhea.
Gastrointestinal Fluid Loss: Vomiting, diarrhea, surgical drainage, and malabsorption can deplete blood volume.
Renal Fluid Loss:Osmotic Diuresis: Conditions like diabetes mellitus and hypoadrenalism lead to excessive urine production, depleting blood volume.
Sequestration in High Vascular Areas: Conditions like pancreatitis and trauma can cause fluid accumulation in certain areas, leading to decreased blood volume circulating to the kidneys.

2. Low Cardiac Output:

Causes:

Myocardial Diseases: Heart muscle diseases like heart failure, cardiomyopathy, and myocardial infarction can reduce the heart’s ability to pump blood effectively.
Valvular Diseases: Diseases of the heart valves, like stenosis or regurgitation, can obstruct blood flow and reduce cardiac output.
Pericardial Diseases: Pericarditis, pericardial effusion, and cardiac tamponade can restrict heart function, leading to reduced cardiac output.
Arrhythmias: Irregular heartbeats can compromise the efficiency of blood pumping.
Pulmonary Hypertension: High blood pressure in the lungs increases the workload on the heart, potentially leading to reduced cardiac output.
Massive Pulmonary Embolism: Blood clots in the lungs can block blood flow, reducing cardiac output.
Septic Shock: Severe infection can lead to widespread vasodilation and reduced blood pressure, compromising blood flow to the kidneys.

B. Intrarenal/Intrinsic Renal Causes:

This category involves direct damage to the kidney tissue itself, often triggered by inflammatory or immunological responses.

1. Toxins:

Nephrotoxic Drugs:

Aminoglycosides: Antibiotics like streptomycin and gentamicin can cause direct damage to kidney tubules.
Rifampicin: An anti-tuberculosis drug that can be nephrotoxic.
Tetracycline: An antibiotic that can cause kidney damage, particularly in children.
Other Nephrotoxins: Contrast dyes, certain chemotherapy drugs, and NSAIDs (non-steroidal anti-inflammatory drugs) can also damage the kidneys.

Heavy Metals: Exposure to heavy metals like phenol, carbon tetrachloride, and chlorates can cause significant kidney damage.

Endogenous Toxins:

Hemolysis: Destruction of red blood cells, often due to Rh incompatibility, releases toxic substances that can damage the kidneys.
Uric Acid Oxalates: High levels of uric acid and oxalates in the blood can form crystals that damage kidney tissue.

2. Diseases of the Glomeruli:

Glomerulonephritis: Inflammation of the glomeruli, the tiny filtering units in the kidneys. This can be caused by infections, autoimmune diseases, or other factors.
Pyelonephritis: Infection of the kidneys and the pelvis of the kidneys.

3. Acute Tubular Necrosis:

Causes: Damage to the tubules, the functional units of the kidneys, can be caused by toxins, ischemia, or other factors. This leads to impaired reabsorption and secretion of fluids and electrolytes.

4. Vasculitis: Inflammation of the blood vessels in the kidneys can damage the filtering units and reduce blood flow.

C. Post-Renal Causes:

This category involves obstruction of the urinary outflow tract, preventing urine from being drained from the kidneys.

Causes:

Tumors: Tumors in the bladder, prostate, or other parts of the urinary tract can block urine flow.
Stones: Kidney stones or bladder stones can obstruct the flow of urine.
Edema: Swelling in the urinary tract, often due to infection or inflammation, can obstruct urine flow.
Prostatic Hyperplasia: Enlargement of the prostate gland can compress the urethra, blocking urine flow.
Other Obstructions: Urethral strictures, congenital abnormalities, and trauma can also cause urinary outflow obstruction.

Phases/Stages of Acute Renal Failure

There are four phases of Acute Renal Failure when Initiation phase is included, otherwise they are 3 stages that begin with Oliguria

Initiation(Onset)or Asymptomatic Phase: The initiation period begins with the initial insult, and ends when oliguria develops. Period from the initial insult until signs/symptoms become apparent. Kidney injury is evolving. Early intervention here can prevent progression. Lasts hours to days. In the early stages of renal failure, often referred to as the asymptomatic phase, the kidneys start to lose their function, but individuals may not experience any noticeable symptoms. This phase can last for months or even years, and kidney damage may progress gradually without apparent signs.
Oliguric Phase/ Oliguria. This stage is characterized by reduced urine output of <400mls/day. This phase lasts 1-2 weeks. The oliguria period is accompanied by an increase in the serum concentration of substances usually excreted by kidneys. Other symptoms that may manifest during this phase include fatigue, fluid retention leading to edema (swelling), electrolyte imbalances, high blood pressure, and a buildup of waste products in the blood. Significant fall in GFR and urine output (<400 mL/day). Accumulation of fluid, electrolytes (K+, Phos), and waste products (BUN, Cr). Metabolic acidosis worsens. Complications are most likely during this phase.
Diuretic Phase/ Diuresis. Urine output increases to as much as 4000 mL/day but no waste products, at the end of this stage you may begin to see improvement. The diuresis period is marked by a gradual increase in urine output, which signals that glomerular filtration has started to recover. GFR starts to rise, BUN/Cr start to fall (lagging behind urine output). Patient is at risk for dehydration and electrolyte losses (hypokalemia, hyponatremia). Lasts approximately 1-3 weeks.
Recovery. The recovery period signals the improvement of renal function and may take 3 to 12 months. If it is insufficient, it develops to Chronic renal failure. GFR increases, and tubular function normalizes. BUN and creatinine levels return towards baseline. Some patients recover fully, while others may have residual kidney damage or progress to CKD.

However, it’s important to note that not all cases of renal failure have a recovery phase, especially in chronic kidney disease (CKD), where kidney damage tends to be irreversible.

● End-Stage Renal Disease (ESRD): If renal failure progresses to a point where the kidneys are functioning at less than 10-15% of their normal capacity, it is referred to as end-stage renal disease (ESRD). At this stage, kidney function is severely compromised, and individuals require renal replacement therapies such as dialysis or kidney transplantation to sustain life.

Clinical features of Acute Renal Failure

Acute renal failure (ARF) is a sudden decline in kidney function, leading to a buildup of waste products in the blood and a disruption in fluid and electrolyte balance.

1. Reduced Urine Output (Oliguria): Occurs within 1-3 days, a rapid decrease in urine output occurs, often accompanied by a significant rise in blood urea nitrogen (BUN) and creatinine levels.

Duration: This phase, known as the oliguric phase, can persist for 7-20 days, depending on the severity and underlying cause of ARF.
Mechanism: The kidneys are unable to effectively filter waste products and excess fluids from the bloodstream, leading to their accumulation.

2. Electrolyte Imbalance:

Hyperkalemia: Increased potassium levels in the blood due to the kidneys’ inability to excrete potassium efficiently. This can lead to potentially life-threatening cardiac arrhythmias.
Other imbalances: Sodium, calcium, and phosphate levels may also be affected, contributing to various symptoms.

3. Fluid Imbalance:

Generalized Edema: Fluid retention due to decreased urine output can cause swelling in the legs, ankles, feet, and even the lungs (pulmonary edema).

4. Gastrointestinal Symptoms:

Decreased Appetite: Nausea and vomiting are common due to the accumulation of toxins in the body and electrolyte disturbances.

5. Lethargy and Fatigue:

Weakness and drowsiness: The body’s energy levels are depleted due to impaired kidney function and electrolyte imbalances.

6. Central Nervous System (CNS) Symptoms:

Drowsiness, headache, confusion: Accumulation of toxins in the bloodstream can affect brain function.
Muscle twitching, seizures/convulsions: Severe electrolyte imbalances, particularly hyperkalemia, can lead to seizures.

7. Pallor:

Pale skin: Anemia, a common complication of ARF, can cause pallor due to the kidneys’ inability to produce erythropoietin, a hormone essential for red blood cell production.

8. Pulmonary Edema:

Dyspnea (shortness of breath): Fluid accumulation in the lungs can make breathing difficult.

9. Dehydration:

Dryness of skin and mucous membranes: Reduced fluid intake and inability to excrete waste products lead to dehydration, manifesting as dry skin and mucous membranes.

10. Cardiovascular Signs:

Congestive heart failure: Fluid overload and electrolyte disturbances can strain the heart, leading to heart failure.
Severe hypertension: Decreased kidney function can contribute to high blood pressure, potentially leading to complications such as stroke.

Investigations/Diagnostic Findings

Urine

Volume: Usually less than 100 mL/24 hours (anuric phase) or 400 mL/24 hours (oliguric phase)
Color: Dirty, brown sediment indicates the presence of RBCs, hemoglobin.
Specific gravity: Less than 1.020 reflects kidney disease, e.g., glomerulonephritis, pyelonephritis.
Protein: High-grade proteinuria (3–4+) strongly indicates glomerular damage when Red Blood Cells and casts are also present
Glomerular filtration rate (GFR): The GFR is a standard means of expressing overall kidney function.

Blood

Serum Creatinine & BUN(BUN/Cr): Elevated,BUN:Cr ratio can sometimes help differentiate causes (>20:1 suggests prerenal).
Complete blood count (CBC): Hemoglobin (Hb) decreased in presence of anemia.
Arterial blood gases (ABGs): Metabolic acidosis (pH less than 7.2) may develop because of decreased renal ability to excrete hydrogen and end products of metabolism.
Chloride, phosphorus, and magnesium, Sodium, Potassium: Elevated related to retention and cellular shifts (acidosis) or tissue release (red cell hemolysis).
Estimated GFR (eGFR): Calculated from creatinine, age, sex, race; tracks function over time (less accurate in rapidly changing AKI).

Imaging

Renal ultrasound: Essential first step. Assesses kidney size (small suggests CKD), checks for hydronephrosis (indicating postrenal obstruction), evaluates renal vasculature (Doppler). Determines kidney size and presence of masses, cysts, obstruction in upper urinary tract.
Retrograde pyelogram: Outlines abnormalities of renal pelvis and ureters. ● Renal arteriogram: Assesses renal circulation and identifies extravascularities, masses.
Voiding cystourethrogram: Shows bladder size, reflux into ureters, retention.
Non Nuclear computed tomography (CT) scan: Cross-sectional view of kidney and urinary tract detects presence/extent of disease.
Magnetic resonance imaging (MRI): Provides information about soft tissue damage.
Excretory urography (intravenous urogram or pyelogram): Radiopaque contrast concentrates in urine and facilitates visualization of KUB(Kidney, Ureter, Bladder)

Kidney Biopsy:

Performed when the cause of AKI is unclear after initial workup, especially if intrinsic glomerular disease (GN) or interstitial nephritis (AIN) is suspected.
Involves taking a small sample of kidney tissue via a needle, usually under ultrasound guidance, for microscopic examination. Helps guide specific treatment.

Management of Acute Renal Failure

Aims:

Primary Goal: Identify and treat the underlying cause promptly!

Prerenal: Restore renal perfusion (fluids, blood products, improve cardiac output).
Intrarenal: Stop nephrotoxic agents, treat underlying infection/inflammation (e.g., steroids for AIN/some GN), supportive care for ATN.
Postrenal: Relieve the obstruction (e.g., Foley catheter for bladder outlet obstruction, ureteral stents, nephrostomy tubes).
Restore Normal Chemical Balance: The primary goal is to stabilize electrolytes, acid-base balance, and fluid volume within safe ranges.
Prevent Complications: Prevent or manage complications that can arise during the course of acute renal failure, such as fluid overload, electrolyte disturbances, hypertension, and infections, until renal function recovers.

In-Hospital Management:

1. Admission and Rest: Admit the patient to a monitored setting and ensure adequate rest to minimize energy expenditure. Assist with daily activities to conserve energy.

2. Fluid and Salt Restriction:

Fluid Restriction: Limit fluid intake to 600 ml per day plus the previous day’s fluid loss. This helps prevent fluid overload and edema.
Salt Restriction: Limit salt intake to less than 2 grams per day (about half a teaspoon). This reduces fluid retention and helps control blood pressure.

3. Fluid Balance Monitoring:

Fluid Balance Chart: Accurately monitor fluid intake and output (urine, vomit, diarrhea) using a fluid balance chart to assess fluid balance and adjust fluid intake accordingly.
Overload Prevention: Avoid overloading the patient with fluids by adjusting fluid intake based on the individual’s needs and fluid losses.

4. Edema Assessment:

Edema Monitoring: Regularly assess for edema (swelling) in the extremities, skin turgor, and fontanelles (in infants) to identify fluid overload or dehydration.

5. Symptom Management:

Antiemetics (ondansetron, metoclopramide – dose adjust) for nausea, laxatives for constipation, anticonvulsants (levetiracetam often preferred due to renal clearance profile) if seizures occur. Vitamin supplements may be needed if nutrition poor.

6. Vital Signs Monitoring:

Blood Pressure: Monitor blood pressure twice daily to detect hypertension or hypotension. Antihypertensives if needed, avoiding agents that worsen renal perfusion in certain settings (e.g., ACEi/ARBs if bilateral RAS suspected). Low dose dopamine is NOT recommended for renal protection/vasodilation – proven ineffective.
Weight: Weigh the patient twice daily to assess fluid balance.
Other Vital Observations: Monitor other vital signs such as temperature, heart rate, and respiratory rate.

7. Dialysis:Dialysis (Renal Replacement Therapy – RRT): Used when supportive measures fail to control life-threatening complications. Removes waste products, excess fluid, and corrects electrolyte/acid-base imbalances. Dialysis is considered in severe cases to address:

Fluid Overload: Dialysis can help remove excess fluid, reducing edema, pulmonary edema, and congestive heart failure.
Hyperkalemia (High Potassium Levels): Dialysis removes excess potassium from the blood, preventing potentially life-threatening complications.
Elevated BUN (Blood Urea Nitrogen): Dialysis can help lower elevated BUN levels, a marker of kidney function.
Severe Hypertension: Dialysis can help control severe hypertension that is not responsive to medications.
Metabolic Acidosis: Dialysis can help correct metabolic acidosis, a condition where the body produces too much acid.

Types of Dialysis:

Hemodialysis: This involves filtering the blood through a machine outside the body.
Peritoneal Dialysis: This involves using the patient’s peritoneal membrane (lining of the abdomen) as a filter.

Indications of Dialysis (AEIOU mnemonic):

Acidosis: Severe metabolic acidosis refractory to bicarbonate therapy.
Electrolytes: Severe, refractory hyperkalemia.
Intoxications: Dialyzable drug overdoses or toxins (e.g., methanol, ethylene glycol, lithium, salicylates).
Overload: Fluid overload refractory to diuretics, causing respiratory compromise.
Uremia: Symptomatic uremia (encephalopathy, pericarditis, severe bleeding).

8. Fluid and Electrolyte Replacement/Management:

Fluid Management: Critical. Requires meticulous monitoring of intake (oral, IV) and output (urine, drains, GI losses) plus estimation of insensible losses (~500-1000 mL/day). Aim for euvolemic (normal fluid balance). Fluid restriction is often needed in the oliguric phase. Careful IV fluid selection (isotonic preferred, avoid potassium-containing fluids if hyperkalemic). In diuretic phase, it may need significant fluid replacement to prevent dehydration. Daily weights are essential.
Electrolyte Correction: Monitor and replace/restrict electrolytes (Na+, K+, Ca++, Phos) as needed based on lab values.

9. Nutritional Therapy:

Goal: Provide adequate calories to prevent catabolism (muscle breakdown, which increases BUN), while managing electrolyte and fluid restrictions.
Consultation: Renal dietitian consultation is highly recommended. Enteral or parenteral nutrition may be required if oral intake is inadequate.
Calories: High calorie intake often needed due to hypermetabolic state, especially in critical illness. Primarily carbohydrates and fats.
Protein: Needs are controversial in AKI. Severe restriction may hinder tissue repair. Moderate intake (0.8-1.2 g/kg/day) often recommended, may increase with dialysis. Needs individualized based on catabolic state and dialysis modality. Moderate protein intake, but provide adequate calories to meet energy needs. Protein restriction helps reduce the burden on the kidneys.
Electrolyte Restrictions: Potassium, phosphate, and sodium intake usually need to be limited, especially in the oliguric phase.

Low-potassium foods: Apples, berries, cabbage, carrots, green beans, grapes, rice.
Avoid high-potassium foods: Bananas, oranges, potatoes, tomatoes, spinach, dried fruits, salt substitutes.

Diet Considerations: Consider a balanced diet with adequate calories and vitamins, limiting foods high in potassium, sodium, and phosphorus.

10. Electrolyte and Urine Monitoring:

Electrolytes: Frequently check electrolyte levels (sodium, potassium, calcium, magnesium) to identify and correct imbalances.
Urine Output: Monitor urine output closely to assess kidney function and adjust treatment as needed.

11. Infection Treatment:

Antibiotics if infection is present/suspected. Choose agents carefully and adjust doses based on estimated renal function (eGFR). Prefer antibiotics not primarily cleared by the kidneys if possible (e.g., some macrolides like azithromycin, chloramphenicol, doxycycline) or those easily dose-adjusted.

12. Complications Management:

Hypertension: Administer antihypertensive medications to control blood pressure.
Convulsions: Treat seizures with anticonvulsant medications.
Infections: Promptly treat any infections with appropriate antibiotics.

13. Metabolic Acidosis:

Sodium Bicarbonate: Administer sodium bicarbonate 50-100 mcg to correct metabolic acidosis, which occurs when the body produces too much acid. IV Sodium Bicarbonate may be given for severe acidosis (pH < 7.1-7.2 or HCO3 < 10-12), but use cautiously due to sodium/fluid load. Dialysis corrects acidosis effectively.
Sodium Bicarbonate Mechanism: Sodium bicarbonate helps restore the acid-base balance in the body, reducing the excess acid.

14. Hyperkalemia Management:

IV Dextrose 50%, Insulin, and Calcium: Administer intravenous dextrose 50%, insulin, and calcium replacement to shift potassium back into cells, lowering blood potassium levels.
Diuretic Agents: Diuretic agents can also be used to control fluid volume and aid in potassium excretion.
Antagonize Cardiac Effects: IV Calcium Gluconate or Calcium Chloride (stabilizes cardiac membrane, does not lower K+).
Shift K+ into Cells: IV Insulin with Glucose, Sodium Bicarbonate (if acidotic), Beta-agonists (albuterol nebulized).
Remove K+ from Body: Potassium-binding resins (e.g., Sodium Polystyrene Sulfonate (Kayexalate), Patiromer, Sodium Zirconium Cyclosilicate), Loop Diuretics, Dialysis (most effective).

15. Skin Integrity:

Pressure Area Care: Provide proper care of pressure areas to prevent skin breakdown, particularly in severely ill patients.
Regular Turning: Turn patients regularly to relieve pressure points and promote circulation.

16. Nephrotoxic Drug Suspension:

Stop Nephrotoxic Drugs: Stop any medications that may be toxic to the kidneys (nephrotoxic drugs).

17. Shock Management:

Hemorrhagic Shock: Treat shock with blood transfusions in cases of hemorrhagic shock to replace blood loss.

Nursing Management of AKI:

Assessment:

Frequent vital signs (BP, HR, RR, Temp).
Strict Intake & Output (often hourly). Calculate fluid balance.
Daily weights (same time, scale, clothing).
Assess for fluid overload: Edema, JVD, lung sounds (crackles), shortness of breath, S3 heart sound.
Assess for dehydration (especially diuretic phase): Skin turgor, mucous membranes, orthostatic hypotension.
Monitor lab results: BUN, Cr, electrolytes (esp. K+), ABGs, CBC. Report critical values promptly.
ECG monitoring for signs of hyperkalemia (peaked T waves, wide QRS).
Assess mental status, neurological checks.
Monitor for signs of infection (fever, tachycardia, site redness/drainage).
Assess nutritional status, appetite, GI symptoms.
Skin integrity assessment (risk of breakdown due to edema, immobility).
Assess dialysis access site (catheter) if present.

Nursing Diagnoses:

Fluid Volume Excess (related to decreased GFR/urine output, sodium retention).
Risk for Deficient Fluid Volume (related to excessive loss during diuretic phase).
Risk for Decreased Cardiac Output (related to fluid overload, electrolyte imbalance, acidosis).
Inadequate nutrition (related to anorexia, nausea, dietary restrictions, catabolism).
Risk for Infection (related to uremia, invasive lines/procedures).
Risk for Electrolyte Imbalance (Hyperkalemia, Hypocalcemia, etc.).
Decreased Activity tolerance (related to anemia, uremia, fluid imbalance).
Excessive Anxiety (related to critical illness, uncertain prognosis).
Knowledge Deficit (regarding condition, treatment, diet).

Interventions:

Administer medications as ordered, monitoring for effects and side effects. Adjust doses based on renal function.
Implement fluid restrictions/replacements accurately. Maintain IV therapy.
Monitor patient response to diuretics and dialysis.
Maintain meticulous aseptic technique with all lines and procedures. Catheter care.
Monitor for and prevent complications (hyperkalemia, fluid overload, infection, bleeding, skin breakdown).
Provide nutritional support, assist with meals, monitor intake.
Frequent repositioning, skin care.
Provide patient and family education about AKI, treatments, diet, and follow-up.
Provide emotional support and reassurance.
Collaborate with multidisciplinary team (physicians, dietitians, pharmacists, social workers).

CHRONIC RENAL FAILURE

CKD is defined as abnormalities of kidney structure or function, present for more than 3 months, with implications for health. It involves a progressive, slow, insidious, and irreversible decline in renal excretory and regulatory functions.

Criteria: Either GFR < 60 mL/min/1.73 m² for >3 months, OR markers of kidney damage (e.g., albuminuria [ACR ≥ 30 mg/g], urine sediment abnormalities, electrolyte abnormalities due to tubular disorders, histological abnormalities, structural abnormalities on imaging, history of kidney transplant) present for >3 months.

Chronic Kidney Disease (CKD): The broader term encompassing all stages of chronic kidney damage/reduced function.

Chronic Renal Failure (CRF): Often used to describe later stages of CKD when GFR is significantly reduced and complications are prominent.

End-Stage Renal Disease (ESRD): The final stage (Stage 5 CKD), where kidney function is insufficient to sustain life, requiring renal replacement therapy (dialysis or transplantation). GFR is typically < 15 mL/min/1.73 m². This stage is characterized by uremia, the syndrome of symptoms resulting from the accumulation of toxic waste products.

Causes of Chronic Renal Failure:

Major Causes:

Diabetes Mellitus (Diabetic Nephropathy): Leading cause (~40-50%). High blood glucose damages glomerular capillaries.
Hypertension (Hypertensive Nephrosclerosis): Second leading cause (~25-30%). High blood pressure damages small blood vessels in the kidneys.

Other Causes:

Glomerulonephritis: Chronic inflammation of the glomeruli (e.g., IgA nephropathy, FSGS).
Polycystic Kidney Disease (PKD): Inherited disorder causing multiple cysts in the kidneys.
Chronic Pyelonephritis: Recurrent kidney infections causing scarring.
Chronic Tubulointerstitial Nephritis: Long-term damage to tubules/interstitium (e.g., from drugs like lithium, chronic NSAID use, heavy metals).
Obstructive Uropathy: Long-term blockage (e.g., untreated BPH, congenital anomalies).
Vascular Diseases: Renal artery stenosis, atheroembolic disease.
Autoimmune Disorders: Systemic Lupus Erythematosus (SLE), scleroderma, vasculitis.
Nephrotoxic Agents (Long-term exposure): Certain medications, heavy metals.
Kidney Stones (Nephrolithiasis): Recurrent stones can cause damage/obstruction.
Congenital Abnormalities: Structural kidney problems present from birth.
Risk Factors: Family history of kidney disease, older age, ethnicity (African American, Hispanic, Native American, Asian American have higher risk), obesity, smoking, cardiovascular disease.

Pathophysiology of CKD Progression:

Initial Kidney Damage: Due to underlying etiology (diabetes, HTN, etc.).
Nephron Loss: Gradual destruction of functioning nephrons.
Compensatory Hypertrophy & Hyperfiltration: Remaining nephrons enlarge and increase their individual filtration rate to compensate for the loss. This maintains overall GFR initially.
Intraglomerular Hypertension: Increased pressure and flow within the remaining glomeruli.
Maladaptive Consequences: This hyperfiltration, while initially compensatory, eventually becomes damaging. It leads to further glomerular injury (glomerulosclerosis), proteinuria, and interstitial fibrosis.
Progressive Nephron Loss: A vicious cycle ensues where compensation leads to further damage and loss of more nephrons.
Declining GFR: As nephron mass falls below a critical level, overall GFR begins to decline steadily.
Uremia: When GFR falls significantly (typically <15-20 mL/min), waste products accumulate to toxic levels, and regulatory functions fail, leading to the clinical syndrome of uremia affecting multiple organ systems.

Stages of CKD (Based on GFR and Albuminuria – KDIGO Guidelines): Staging helps guide management.

Stage	GFR (mL/min/1.73 m²)	Description	Clinical Action
1	≥ 90	Kidney damage, normal GFR	Diagnose/treat underlying cause, reduce CV risk
2	60-89	Kidney damage, mild ↓ GFR	Estimate progression, continue risk reduction
3a	45-59	Mild-moderate ↓ GFR	Evaluate & treat complications (anemia, bone disease)
3b	30-44	Moderate-severe ↓ GFR	More aggressive complication management
4	15-29	Severe ↓ GFR	Prepare for Renal Replacement Therapy (RRT)
5	< 15 (or dialysis)	Kidney Failure (ESRD)	RRT (Dialysis or Transplant) required for survival

(Albuminuria is also staged: A1 <30, A2 30-300, A3 >300 mg/g creatinine – higher albuminuria indicates higher risk at any GFR stage)

Clinical Manifestations of CKD (Uremic Syndrome)

Develop gradually as GFR declines, affecting nearly every organ system. Many symptoms are nonspecific initially.

Neurological:

Early: Fatigue, lethargy, impaired concentration, irritability, depression, sleep disturbances.
Late: Peripheral neuropathy (restless legs syndrome, burning feet, paresthesias), asterixis, muscle twitching, encephalopathy (confusion, disorientation, memory loss), seizures, coma.
Cognitive impairment is common.

Cardiovascular (Leading cause of death in CKD):

Hypertension: Very common (due to fluid/sodium retention, RAAS activation).
Heart Failure: Due to volume overload, hypertension, anemia, uremic cardiomyopathy.
Left Ventricular Hypertrophy (LVH).
Arrhythmias: Especially due to hyperkalemia, hypocalcemia, structural changes.
Pericarditis: Inflammation of the pericardial sac due to uremic toxins. Can lead to pericardial effusion and tamponade.
Accelerated Atherosclerosis: Increased risk of MI, stroke, peripheral vascular disease (due to traditional risk factors plus inflammation, oxidative stress, lipid abnormalities, Ca/Phos issues).
Pitting Edema: Due to fluid retention.

Hematologic:

Anemia: Normocytic, normochromic. Primarily due to decreased erythropoietin (EPO) production by failing kidneys. Iron deficiency (absolute or functional) and B12/folate deficiency can contribute. Causes fatigue, weakness, pallor, reduced exercise tolerance.
Bleeding Tendency: Platelet dysfunction (impaired adhesion/aggregation) due to uremic toxins. Leads to easy bruising, prolonged bleeding time.
Impaired Immune Function: Increased susceptibility to infections (WBC dysfunction).

Gastrointestinal:

Anorexia, nausea, vomiting (especially in the morning).
Uremic Fetor: Ammonia-like odor on the breath (breakdown of urea in saliva).
Metallic taste (dysgeusia).
Mouth ulcerations (stomatitis), bleeding gums.
Constipation or diarrhea.
GI bleeding (uremic gastritis/colitis, platelet dysfunction).

Pulmonary:

Pulmonary edema (“uremic lung” on CXR) due to fluid overload. Causes dyspnea, orthopnea, crackles.
Pleuritis/Pleural effusion (similar mechanism to pericarditis).
Kussmaul respirations (deep, rapid breathing) due to severe metabolic acidosis.
Thick, tenacious sputum. Increased risk of pneumonia.

Metabolic / Endocrine:

Metabolic Acidosis: Impaired acid excretion and bicarbonate regeneration.
Electrolyte Imbalances: Hyperkalemia, Hyperphosphatemia, Hypocalcemia (late), Hypermagnesemia (less common unless intake high). Sodium may be high/low/normal.
Carbohydrate Intolerance: Insulin resistance, impaired insulin degradation (may lead to lower insulin needs in diabetics as CKD progresses).
Hyperlipidemia: Altered lipid metabolism (high triglycerides, low HDL).
Secondary Hyperparathyroidism: Complex process: ↓GFR → ↑Phosphate → ↓Calcium (binds phosphate) & ↓Active Vit D → ↑Parathyroid Hormone (PTH) secretion → PTH tries to ↑Calcium and ↓Phosphate by acting on bone and kidney → Leads to Renal Osteodystrophy.

Musculoskeletal:

Renal Osteodystrophy: Bone disease resulting from Ca/Phos/VitD/PTH imbalances. Includes osteitis fibrosa cystica (high turnover bone disease due to high PTH), osteomalacia (low turnover), adynamic bone disease (low turnover). Causes bone pain, increased fracture risk, muscle weakness.

Dermatologic:

Generalized itching (Pruritus): Common and distressing. Cause multifactorial (uremic toxins, dry skin, high Phos/PTH).
Dry skin (xerosis).
Pallor (due to anemia).
Ecchymoses (easy bruising) due to platelet dysfunction.
“Uremic Frost“: Crystallized urea deposits on skin (rare now with earlier dialysis).
Thin, brittle nails; thin, dry hair.

Genitourinary / Reproductive:

Early: Nocturia (loss of concentrating ability).
Late: Oliguria or Anuria.
Sexual dysfunction: Decreased libido, erectile dysfunction (men), menstrual irregularities/infertility (women).

Diagnostic Evaluations for CKD:

Blood Tests: BUN, Creatinine (monitor trends, calculate eGFR), Electrolytes (K, Na, Cl, HCO3, Ca, Phos), Magnesium, Parathyroid Hormone (PTH), Vitamin D levels, CBC (anemia), Iron studies (ferritin, TSAT), Lipid profile, Albumin (nutritional status), HbA1c (if diabetic).
Urine Tests: Urinalysis (protein, blood, glucose, sediment for casts), Urine Albumin-to-Creatinine Ratio (ACR) (quantifies albuminuria – key marker of damage and risk), 24-hour urine collection (for measured CrCl or protein – less common now).
Renal Biopsy: Sometimes performed if the cause of CKD is unclear, especially if a treatable condition like certain glomerulonephritides is suspected. Less common than in AKI.
CBC: Assess for anemia.
Imaging Studies:

Renal Ultrasound: Assess kidney size (typically small and echogenic in CKD, except in PKD or diabetic nephropathy where they can be normal/large initially), rule out obstruction, evaluate for cysts/masses.
CT/MRI: Less routine, used for specific indications (e.g., suspected malignancy, complex anatomy)

Management of CKD

Aims of Management

Focuses on slowing progression, managing complications, and preparing for RRT. Requires a multidisciplinary approach.

1. Slowing Progression:

Blood Pressure Control: Strict control is crucial! Target typically <130/80 mmHg (may vary). ACE inhibitors or ARBs are often first-line, especially in patients with proteinuria/albuminuria, due to renoprotective effects beyond BP lowering.
Glycemic Control: Tight control in diabetics (target HbA1c ~7% or individualized). SGLT2 inhibitors and GLP-1 agonists have shown significant renoprotective benefits in diabetic kidney disease.
Treat Underlying Cause: Address glomerulonephritis, infections, obstruction if possible.
Avoid Nephrotoxins: NSAIDs, contrast dye (if possible), certain antibiotics.
Smoking Cessation.
Weight Management.

2. Managing Complications:

Fluid & Sodium Management: Sodium restriction (usually <2g/day), fluid restriction may be needed in later stages if edema/hypertension present. Loop diuretics (furosemide) often required.
Hyperkalemia: Dietary potassium restriction, review medications (stop K-sparing diuretics, ACEi/ARBs may need dose adjustment/caution), potassium binders (patiromer, sodium zirconium cyclosilicate) for chronic management.
Metabolic Acidosis: Oral alkali therapy (sodium bicarbonate or sodium citrate) if serum bicarbonate falls consistently below 22 mEq/L.
Hyperlipidemia: Statins recommended for cardiovascular risk reduction.
Cardiovascular Disease Prevention: Manage BP, lipids, glucose; aspirin (if indicated); lifestyle modifications.
Mineral and Bone Disorder (CKD-MBD):
Phosphate Control: Dietary phosphate restriction, Phosphate binders taken with meals (Calcium carbonate/acetate initially; non-calcium binders like sevelamer, lanthanum preferred if calcium high or vascular calcification present).
Calcium/Vitamin D: Maintain normal calcium levels. Vitamin D supplementation (often active form like calcitriol or analogues) if deficient and PTH high. Avoid excessive calcium intake.
PTH Control: Use Vitamin D analogues, Calcimimetics (e.g., cinacalcet – increases sensitivity of calcium-sensing receptor on parathyroid gland) to lower PTH if severely elevated despite other measures. Parathyroidectomy in refractory cases.
Anemia:
Rule out/treat iron deficiency (oral or IV iron).
Erythropoiesis-Stimulating Agents (ESAs) like epoetin alfa, darbepoetin alfa to stimulate RBC production. Target hemoglobin typically 10-11.5 g/dL (higher targets associated with risks).

Medications

Antibiotics:

– Class: Antibiotics are medications used to treat bacterial infections.

– Examples: Common antibiotics used for kidney infections include fluoroquinolones (e.g., ciprofloxacin, levofloxacin), cephalosporins (e.g., ceftriaxone, cephalexin), and

trimethoprim/sulfamethoxazole.

– Side Effects: Potential side effects may include gastrointestinal upset, allergic reactions, rash, photosensitivity, and rarely, serious adverse events like tendon rupture (in the case of fluoroquinolones).

– Contraindications: Contraindications may include known allergies to the medication, certain medical conditions, or interactions with other medications. It’s important to discuss your medical history and current medications with your healthcare provider.

Analgesics:

– Class: Analgesics are medications used to relieve pain.

– Examples: Nonsteroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen or acetaminophen (paracetamol) may be used for pain relief in kidney infections or diseases.

– Side Effects: Common side effects of NSAIDs include gastrointestinal upset, stomach ulcers, and kidney problems if used excessively or for a prolonged period. Acetaminophen should be used cautiously in patients with underlying liver disease or if taken in excessive amounts.

– Contraindications: Contraindications may include known allergies to the medication, certain medical conditions (e.g., gastric ulcers, liver disease), or interactions with other medications. Discuss your medical history and current medications with your healthcare provider.

Diuretics:

– Class: Diuretics are medications that increase urine output and help remove excess fluid from the body.

– Examples: Diuretics commonly used in kidney diseases include loop diuretics (e.g., furosemide) and thiazide diuretics (e.g., hydrochlorothiazide).

– Side Effects: Common side effects may include electrolyte imbalances, dehydration, dizziness, and increased urination.

– Contraindications: Contraindications may include known allergies to the medication, certain medical conditions (e.g., severe electrolyte imbalances, kidney failure), or interactions with other medications. Your healthcare provider will assess your specific situation.

3. Nutritional Therapy:

Protein: Moderate protein restriction (e.g., 0.6-0.8 g/kg/day) may help slow progression in pre-dialysis stages (controversial, needs careful monitoring to avoid malnutrition). Once on dialysis, protein needs increase (1.0-1.2 g/kg/day for HD, higher for PD) due to losses during treatment.
Calories: Ensure adequate caloric intake (25-35 kcal/kg/day) to prevent catabolism.
Sodium, Potassium, Phosphate: Restrictions individualized based on lab values and stage.
Fluid: Restriction often necessary in later stages/on dialysis.
Vitamins: Water-soluble vitamins (B complex, C) may need supplementation, especially with dialysis losses. Avoid high doses of Vitamin A (fat-soluble, accumulates).
Requires Renal Dietitian: Essential for education and meal planning.

4. Preparation for Renal Replacement Therapy (RRT):

Initiate discussions and education about RRT options (hemodialysis, peritoneal dialysis, transplantation) ideally in Stage 4 CKD.
Timely placement of dialysis access (AV fistula/graft for HD, PD catheter for PD) well before RRT is needed.
Evaluation for kidney transplantation (living or deceased donor).

5. Renal Replacement Therapy (RRT): Initiated in ESRD (Stage 5).

Hemodialysis (HD): Blood filtered outside the body via a machine. Usually done 3 times/week for 3-5 hours per session, typically in a dialysis center (can be done at home). Requires vascular access (AV fistula preferred, AV graft, or central venous catheter).
Peritoneal Dialysis (PD): Uses the patient’s own peritoneal membrane as the filter. Dialysis fluid (dialysate) is instilled into the abdominal cavity via a surgically placed catheter, dwells for a period, and then drained. Can be done manually several times a day (CAPD) or overnight using a machine (APD). Done at home by the patient.
Kidney Transplantation: Surgical placement of a healthy kidney from a living or deceased donor. Offers the best quality of life and survival but requires lifelong immunosuppression to prevent rejection. Not all patients are suitable candidates.

Nursing Management of CKD:

Focuses on long-term care, education, adherence, monitoring, and supporting the patient through disease progression and RRT.

Assessment:

Monitor vital signs, daily weights, intake/output.
Assess for signs/symptoms of uremia and complications (fluid overload, electrolyte imbalance, anemia, bone disease, neurological changes, cardiovascular issues, infection).
Review lab results (GFR trends, electrolytes, CBC, Ca/Phos/PTH, albumin).
Assess nutritional status, adherence to dietary/fluid restrictions.
Medication reconciliation – ensure appropriate drugs and doses for renal function.
Assess psychosocial status, coping mechanisms, knowledge level.
If on dialysis: Assess access site (fistula/graft: bruit/thrill; PD catheter: exit site infection signs), monitor treatment tolerance.
If post-transplant: Monitor for rejection, infection, medication side effects.

Nursing Diagnoses: Similar to AKI but reflect chronicity.

Fluid Volume Excess.
Inadequate Nutrition intake.
Risk for Infection.
Decreased Activity tolerance.
Risk for Injury (related to bone disease, neuropathy, falls).
Disrupted Body Image (related to access, fluid shifts, skin changes).
Ineffective Coping / Anxiety / Depression.
Knowledge Deficit (complex regimen, RRT options).
Risk for Decreased Cardiac Output.
Risk for Impaired Skin Integrity (related to edema, pruritus, access devices).
Sexual Dysfunction.

Interventions:

Patient Education: Crucial for self-management. Teach about CKD, stages, importance of adherence to diet (Na, K, Phos, fluid, protein limits), medications (purpose, side effects, timing – e.g., phosphate binders with meals), BP/glucose monitoring, recognizing complications, RRT options.
Medication Management: Administer meds, monitor effects, reinforce importance of adherence.
Dietary/Fluid Management: Reinforce dietitian’s recommendations, help patient find acceptable food choices, monitor intake.
Monitoring & Surveillance: Track labs, weights, vitals. Assess for complications.
Symptom Management: Strategies for pruritus (moisturizers, cool baths, antihistamines if ordered), nausea (antiemetics, small frequent meals), fatigue (pacing activities, anemia management).
Access Care: Meticulous care of HD or PD access sites to prevent infection/complications. Teach patient self-care.
Psychosocial Support: Encourage expression of feelings, identify coping strategies, refer to support groups or counseling if needed. Address body image concerns.
Coordination of Care: Collaborate with nephrologist, dietitian, social worker, transplant team, primary care physician.
Promote Activity: Encourage activity as tolerated to maintain strength and well-being.
Prevent Complications: Infection control, fall prevention, skin care

General Nursing Interventions of Renal / kidney diseases

1. Monitor vital signs: Regularly assess and record the patient’s blood pressure, heart rate, respiratory rate, and temperature to detect any changes or abnormalities.

2. Assess fluid status: Monitor the patient’s fluid intake and output, including urine output, to evaluate fluid balance and detect any signs of fluid overload or dehydration.

3. Administer medications as prescribed: Ensure timely administration of prescribed medications, including diuretics, antihypertensives, phosphate binders, erythropoiesis-stimulating agents, and other medications specific to the patient’s condition.

4. Monitor laboratory values: Regularly monitor renal function tests (e.g., serum creatinine, blood urea nitrogen) and electrolyte levels (e.g., sodium, potassium) to assess kidney function and guide treatment decisions.

5. Provide dietary guidance: Collaborate with a registered dietitian to develop an appropriate meal plan, considering the patient’s specific renal disease, stage, and dietary restrictions (e.g., limiting sodium, potassium, phosphorus intake).

6. Assess and manage pain: Evaluate the patient’s pain level, provide appropriate pain management strategies, and monitor the effectiveness of pain relief interventions.

7. Educate about self-care: Teach patients about proper self-care techniques, including medication management, monitoring fluid and dietary restrictions, and recognizing signs of complications or worsening symptoms.

8. Monitor for signs of infection: Be vigilant for signs and symptoms of urinary tract infections (UTIs) or other infections and promptly initiate appropriate treatment if necessary.

9. Assist with dialysis or renal replacement therapy: If the patient requires dialysis or other renal replacement therapies, provide support, educate about the procedure, and monitor for any complications or adverse reactions.

10. Promote physical activity: Encourage patients to engage in regular physical activity within their capabilities to promote overall health, manage weight, and improve cardiovascular fitness.

11. Provide emotional support: Recognize the emotional impact of renal disease on patients and their families, and offer emotional support, counseling, or referrals to support groups or mental health professionals as needed.

12. Monitor and manage fluid balance: Assess for signs of fluid overload or dehydration and collaborate with the healthcare team to adjust fluid management strategies accordingly.

13. Prevent complications: Implement preventive measures to minimize the risk of complications such as pressure ulcers, deep vein thrombosis (DVT), and infections.

14. Monitor and manage electrolyte imbalances: Regularly assess electrolyte levels and implement appropriate interventions to correct imbalances, such as administering electrolyte supplements or adjusting the patient’s diet.

15. Provide wound care: If the patient has surgical wounds or access sites (e.g., arteriovenous fistula, catheter), ensure proper wound care techniques and monitor for any signs of infection or complications.

16. Promote optimal nutrition: Collaborate with the dietitian to optimize the patient’s nutritional status, including ensuring adequate protein intake and addressing any specific dietary needs or restrictions.

17. Educate about medication management: Provide education on the importance of taking medications as prescribed, potential side effects, and the need for regular follow-up appointments.

18. Monitor and manage anemia: Assess and monitor the patient’s hemoglobin and hematocrit levels, collaborate with the healthcare team to manage anemia using appropriate interventions such as iron supplementation or erythropoiesis-stimulating agents.

19. Collaborate with the interdisciplinary team: Work closely with other healthcare professionals, such as nephrologists, social workers, and pharmacists, to ensure comprehensive and coordinated care for the patient.

20. Provide patient and family education: Educate patients and their families about their condition, treatment options, lifestyle modifications, and the importance of adherence to the treatment plan

NB. General guidelines & may vary depending on the specific needs of the patient and the stage and severity of their renal or kidney disease.

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