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Osteomyelitis

Osteomyelitis is a pus forming infection of the bone.

It is among the commonest conditions in children, decreasing as the child grows, and it increases in patients who are immune compromised, mainly aﬀecting older children.

Cause

Children develop infection in a long bone metaphysis. The commonest causative organism is Staphylococcus aureus, following infection elsewhere in the body despite the infrequency of staphylococcal
bacteremia, presumably because of that organism’s particular ability to infect bone

Common causes

Age group	Most common organism
Newborns (less than 4 months	S. aureus ,Enterobacter species & group A&B streptococcus species.
Children (aged 4months to 4yrs )	S. aureus, group A streptococcus species, haemophilus influenza and enterobacter species.
Children 4yrs to adult	S. aureus (80%), groupA streptococcus species, H influenza and enterobacter species
Adult	S. aureus and occasionally Enterobacter or streptococcus species
Sickle cell anemia patients	Salmonella species are the most common in patients with sickle cell disease

Note;

In children the long bone are usually affected. in adults, the vertebrae and the pelvis are most commonly affected.
Acute osteomyelitis invariably occurs in children because of rich blood supply to the growing bones.
When adults are affected it may be because of compromised host resistance due to debilitation, intravenous drug abuse, infectious root canaled teeth or other disease like immunosuppressive.

Wald Vogel Classification of Osteomyelitis

Osteomyelitis can be classified according to;

Duration of Infection
Mechanism of bone infection

Duration of Infection

Acute osteomyelitis ( suppurative osteomyelitis) is usually regarded as that which occurs before there is actual bone death. Initial episodes of Edema, formation of pus, vascular congestion, thrombosis of small vessels, e.t.c
Chronic osteomyelitis (suppurative osteomyelitis phase ) osteomyelitis involves infection both, within and around, the bone that has died. Recurrence of acute cases, Large areas of ischemia, necrosis, and bone sequestra.

N.B.: Acute osteomyelitis can lead to chronic osteomyelitis because without treatment, the infection and inflammation block the blood vessels and causes the bone to die. Chronic osteomyelitis is harder to treat Sequestra= a fragment of dead bone attached to healthy bone

Mechanism of Bone Infection

Hematogenous: Secondary to bacterial transport through the blood. Majority of infections in children
Associated with vascular insufficiency: Infections in patients with diabetes affecting the feet, or peripheral vascular insufficiency
Contiguous: Bacterial inoculation from an adjacent focus. E.g. Posttraumatic Osteomyelitis like from neighboring tissue, infections from prosthetic devices

Pathophysiology of Osteomyelitis

Causative bacteria enters bone causing an infection. Bacteria can enter bone via bloodstream, from a nearby infection, or direct contamination Risk factors include: Open wound over a bone, Open fracture, Recent surgery, Injection around bone, Medications that weaken immune system, Pre-morbid conditions (diabetes).
In general, microorganism may infect the bone through one or more of the three basic methods.
Via the blood stream. (haematogeneously) the most common method. From nearby areas of infection (as in cellulitis )
Penetrating trauma including Iatrogenic causes such as joint replacement or internal fixation of fractures or secondary peripheral periodontitis in teeth
The area usually affected when the infection is contracted through the blood stream is the metaphysis of the bone. Once the bone is infected, leukocytes enter the infected area and in their attempt to engulf the infectious organisms, release enzymes that lyse the bone.
Pus spreads into the bone’s blood vessels, impairing their flow and areas of devitalized infected bone known as sequestra, form basis of chronic infection. Often the body will try to create new bone around the area of necrosis. The resulting new bone is often called an involucium.
On histologic examination these areas of necrotic bone are the basis for distinguishing between acute osteomyelitis and chronic OM
The history is usually short, 48 hours or less. Initially, there is bone pain and marked tenderness without visible inflammation. When infection spreads sub periosteally, local and systemic signs of infection appear. Pus then forms in bone and soft tissues. The appearance of the bone does not change for 10–14 days so radiographs are a baseline for future change and to exclude differential diagnoses (Ewing’s sarcoma, leukaemia). Softening of soft-tissue planes may be seen. OM is all infective process of bone (osseous) component including the bone marrow. When it is chronic, it can lead to bone sclerosis and deformity.

PREDISPOSING FACTORS

Pyomyositis (bacterial infection of muscle)
Cellulitis
Sickle-cell disease (thrombotic crisis)(causative agent mostly S.Aureus, Salmonella also common)
Diabetes
Intravenous drug use
Prior removal of spleen
Age
Immune suppression
Autoimmune disorder
Systemic infections

Signs and Symptoms of Osteomyelitis.

Acute osteomyelitis

Onset is usually over several days
Fever, usually high but may be absent, especially in neonates
Pain (usually severe) in the affected limb
Tenderness and increased “heat” at the site of infection, swelling of the surrounding tissues and joint
Reduced or complete loss of use of the aected limb
The patient is usually a child of 4 years or above with reduced immunity, but adults may also be afected.
History of injury may be given, and may be misleading, especially if there is no fever
Malaise
Redness of the limb
Edema of the limb

Chronic osteomyelitis

May present with pain, erythema, or swelling, sometimes in association with a draining sinus tract
Deep or extensive ulcers that fail to heal after several weeks of appropriate ulcer care (e.g. in diabetic foot), and non-healing fractures, should raise suspicion of chronic osteomyelitis

Deferential diagnosis

Infection of joints
Injury (trauma) to a limb, fracture (children)
Bone cancer (osteosarcoma, around the knee) and adults.

Management of Osteomyelitis

Management can be medical or surgical or both.

Aims of management

To preserve limb and joint function
To prevent further complications

Admission

Child is admitted to pediatric ward.
Patient’s history is taken of including name, sex, address, nationality. Past medical history, past surgical history are taken

Assessment

Vital observation T,P,R and BP and recorded in patients chart

Assessment of patient limb for redness, hotness, edema, general examination of the patient from head to toe
Doctor is informed who will order the following investigations.

Investigations / Diagnosis

Diagnosis is through physical examination, laboratory findings and radiological findings.
¾ X-ray shows
– Nothing abnormal in first 1-2 weeks
– Loss of bone density (rarefaction) at about 2 weeks
– May show a thin “white” line on the surface of the infected part of the bone (periosteal reaction)
– Later, may show a piece of dead bone (sequestrum)
¾ Blood: CBC, ESR, C&S: Type of bacterium may be detected

Medical Management

Immobilize the limb, splint
Elevate the affected limb
Provide pain and fever relief with paracetamol, or ibuprofen
Typically patient need antibiotic for several weeks to properly treat the infections.
Drain the infected site.
Immobilize or stabilize the bone if necessary.
Administer intravenous antibiotics like Cloxacillin Child: below 12yrs 50 mg/kg every 6 hours; Above 12year 500 mg IV every 6 hours for 2 weeks. Then Continue orally for at least 4 weeks (but up to 3 months) if it fails; then,
Ceftriaxone 50mg-100mg/kg for about 10 days, vancomycin, penicillin and ciprofloxacin can also be used depending on results from culture and sensitivity.
Administer analgesics depending on severity like, ibuprofen acetaminophen, morphine for pain relief.
Failure to improve after 48-72 hours of antimicrobial therapy surgical intervention is considered by;
Surgical intervention may be indicated in the following cases: Drainage of subperiosteal , soft tissue abscesses, and intramedullary purulence
Removal of necrotic bone tissue and local pus or drainage is often necessary to speed up healing.
– Debridement of contiguous foci of infection (which also require antimicrobial therapy)
– Excision of sequestra (i.e. weak and lifeless bone) Debridement of the area to remove necrotic tissue.
Failure to improve after 48-72 hours of antimicrobial therapy

Chronic osteomyelitis
Surgery and antibiotics

Continue with the Administration of intravenous antibiotics like ceftriaxone 50mg-100mg/kg for about 10 days, vancomycin, penicillin and ciprofloxacin can also be used depending on results from culture and sensitivity

Nursing Care

Nursing Diagnosis

Ineffective Tissue Perfusion Related to: Inflammatory reaction, Thrombosis of vessels, Tissue destruction, Edema, Abscess formation As evidenced by: Bone necrosis, Continuation of the infectious process, Delayed healing, Pain, Erythema, Swelling, Altered sensation in the affected area, Weak peripheral pulses.

Ineffective Tissue Perfusion Interventions:

1. Establish blood flow at the site.
Blood circulation distributes nutrients throughout the body, aids in controlling waste production, enhances site recovery, and speeds up the healing process. Healthy blood flow across vessels, arteries, veins, and capillaries maximizes perfusion.

2. Manage chronic conditions and lifestyle factors.
Diabetes, peripheral vascular disease, sickle cell disease, neuropathy, smoking, malnutrition, and more affect the revascularization of the affected area. These need to be addressed before surgical intervention.

3. Provide DVT prophylaxis.
Anticoagulants should be administered as ordered to promote circulation and prevent the development of blood clots.

4. Prepare for possible surgery.
Depending on the degree of vascular insufficiency, procedures to restore adequate blood flow, such as debridement or vascular surgery may be necessary.

5. Prevention through pressure ulcer prophylaxis.
Patients who are immobile or bed-bound are at an increased risk of experiencing osteomyelitis due to pressure ulcers. By implementing appropriate interventions such as turning schedules and skin care, this can be prevented.

2. Hyperthermia Related to: Increased metabolic rate, Infection, Inflammatory response, Trauma As evidenced by: Increased body temperature, Warmth to touch, Flushed skin, Tachypnea, Tachycardia

Hyperthermia Interventions:

1. Provide a tepid sponge bath.
Tepid sponge baths lower body temperature and provide comfort to the patient.

2. Apply a cooling blanket.
A cooling blanket can lower the internal body temperature by surface cooling. Monitor closely to prevent a rapid drop in body temp.

3. Initiate antibiotics.
Long-term antibiotics are required for the treatment of osteomyelitis to control the infectious process. Instruct patients that antibiotic therapy may be required for weeks.

4. Instruct on symptoms.
Teach the patient and family that if fever, chills, warmth to the skin, or skin flushing is observed that the body is attempting to fight off infection and to seek immediate assistance.

3. Acute pain Related to: Inflammation, Tissue necrosis As evidenced by: Verbalization of pain, Tenderness with palpation, Guarding behaviors, Facial grimacing, Increased vital signs.

Acute Pain Intervention

1. Reposition as needed.
Repositioning and turning can decrease the stimulation of the pain and pressure receptors.

2. Administer pain medication as prescribed.
Mild or moderate pain may be controlled with non-steroidal anti-inflammatory drugs (NSAIDs). More severe pain or pain related to debridement or surgical intervention may require oral or IV opioid medications.

3. Elevate or immobilize the site.
Elevation or splinting of an extremity may improve pain by increasing circulation.

4. Collaborate with physical and occupational therapists.
Physical and occupational therapists assist in pain management through exercise, stretching, and other techniques.

5. Anticipate referral to a pain specialist.
Osteomyelitis and its treatment can be very painful and prolonged. Acute pain can turn into chronic pain depending on the severity and pain tolerance of the patient, which may need a referral to a pain specialist.

Complications

Necrosis
Gangrene
Amputation
Sepsis
Cancer of the bone.

Osteomyelitis Read More »

Osteopenia of Prematurity

Osteopenia of prematurity is the decrease in the amount of calcium and phosphorus in bones which makes the bones weak and brittle resulting into broken bones.

Prematurity affects bone mineralization and bone growth—thus the condition osteopenia of prematurity;

Normal bone is formed by the deposition of minerals, predominantly calcium (Ca⁺²) and phosphorus (P), onto an organic matrix (osteoid) secreted by the osteoblasts. Osteoclasts play an important role in bone resorption and remodeling.

Osteopenia of prematurity is principally a result of inadequate calcium intake to meet bone growth demands.

Causes

Lack of vitamin D (vitamin D helps in absorption of calcium from intestines and kidneys) by the mother during pregnancy which has to be transferred from the mother to the fetus.
Prematurity these neonates lose much more phosphorous in their urine than babies that are born full-term
Liver problems which may lead to deficiency of vitamin D e.g
cholestasis(obstruction of bile flow).

Signs and symptom

Clinically, osteopenia manifests between 6 and 12 weeks of age and is usually asymptomatic; however, severe manifestations may include the following:

Severe manifestations

1. Poor weight gain and growth failure.
2. Rickets-like findings may include growth retardation, frontal bossing, and epiphyseal widening.
3. Fractures may manifest as pain on handling.
4. Respiratory difficulties or failure to wean off ventilator support due to poor chest wall compliance.

Consequences of osteopenia. Osteopenia can result in myopia of prematurity due to alterations in the shape of the skull. In childhood, infants remain thinner and shorter with a decreased total BMC(Bone Marrow Concentration) and density. Increased urinary calcium excretion has also been reported.

Decreased movements
Swelling of the arm or legs due to unknown fractures.

Pathophysiology

Bone mineralization begins during embryonic phase of human development, but the large part of this process occurs in the third trimester of gestation, during this period .
The most of placental transfer of calcium and phosphorous occurs in the third trimester at the 34th week of gestation .when 80% of the mineral content is stored.
By the 28th week of gestation mineral accumulation is about 60mg/day then increases to more 300mg /day between 35-38th week .
The osteoblast produce the organic bone matrix for deposition of calcium and phosphate with a progressively expansion of bone volume through an increase in trabecular thickness. This This activity is thought to be important for bone development and it helps the baby to grow, If this doesn’t occur the child develops osteopenia of prematurity. Which leads to fractures of long bones including ribs resulting into respiratory insufficiency.
A premature infant may not receive the proper amount of calcium and phosphorus needed to form strong bones.
Premature babies lose much more phosphorus in their urine and they have limited physical activities which lead to weak bones.

Risk Factors

Fetal and neonatal causes

1. Prematurity and birthweight. Preterm birth results in Calcium and Phosphorus deficiency. The frequency of osteopenia is inversely related to gestational age and birthweight. Both conditions predispose these infants to mineral deficiencies in the face of increased nutritional and growth requirements.
2. Feeding practices. Delayed enteral feeding, prolonged use of parenteral nutrition, use of unfortified human milk, enteral feeding restrictions, and malabsorption states can result in mineral deficiencies.
3. Human milk is low in Phosphorus, and donor milk content is even lower compared with preterm maternal milk. Prolonged use can result in low serum phosphate levels and decreased incorporation into the organic bone matrix. Unfortified human milk cannot match the mineral accretion that can be achieved across the placenta.
4. Drugs. Corticosteroids, furosemide, and methylxanthines are commonly used in preterm infants and cause mobilization of Calcium from the bone, resulting in decreased bone mineral content.
5. Lack of mechanical stimulation. Bone growth requires mechanical stimulation that is interrupted by preterm birth, illness, sedation, and paralysis. Neurologically impaired infants with spina bifida have limited mobility and poor bone growth.
6. Vitamin D. Postnatal vitamin D deficiency may occur in breast-fed infants without fortification due to low levels (25–50 IU/L) in breast milk. Other causes of vitamin D deficiency in preterm infants include the following:
  1. Renal (osteodystrophy) disorders.
  2. Drugs such as phenytoin and phenobarbital increase vitamin D metabolism.
7. Aluminum contamination of parenteral nutrition.
8. Malabsorption of vitamin D and Ca⁺² can occur in infants with prolonged cholestasis and short gut syndrome.
Maternal factors
1. Maternal deficiency of vitamin D results in low fetal levels.
2. Maternal smoking, thin body habitus, low Calcium intake, and increased physical activity in the third trimester result in a decreased Calcium in the fetus.
3. Exposure to high doses of magnesium in utero, preeclampsia, chorioamnionitis, and placental infections are associated with osteopenia.
4. Higher incidence of postnatal rickets is seen in infants with intrauterine growth restriction (chronic damage to the placenta may alter phosphate transport).
5. Increased maternal parity and boys have higher incidence.
6. Placental hormones including estrogen and parathyroid hormone (PTH) and PTH-related protein also play a role.

Predisposing factors

Prematurity ;Gestation period of less than 30 weeks
Chronic use of medication that increase mineral excretion e.g diuretics ,theophylline.
Vitamin D deficiency.
Low parathyroid hormone during pregnancy which suppresses the fetal calcium and phosphorous levels.
A less effective intake of calcium and phosphorous occurs in infants with Poor tolerance to Enteral feeds with low mineral content who require total parenteral nutrition.
Common neonatal morbidities like sepsis, acidosis, necrotizing enterocolitis can impair bone remodeling by reducing osteoclast activity, decreasing calcium absorption and increasing calcium renal excretion.
Paralysis may increase calcium renal excretion.
Short gut syndrome(malabsorption of vitamin D and calcium

Diagnosis and Investigations

Radiographs. Most commonly, osteopenia is recognized on radiographs, which are often subjective.

Calcium levels may remain normal until late in the course.

Phosphorous. Serum phosphate levels are low (<3 mg/dL).

Ultrasound. Ultrasound offers several advantages, including easy accessibility and lack of exposure to ionizing radiation. It uses peripheral sites such as the calcaneus and tibia. It measures both qualitative and quantitative bone properties, such as bone mineralization and cortical thickness, respectively, in addition to bone mass (osteopenia), elasticity, and microarchitecture.

Dual-energy x-ray absorptiometry (DEXA). DEXA is the gold standard used to assess both bone size and bone mineral status and can predict risk of fractures in newborn infants. However, limitations in its use and interpretation of data preclude wide clinical application.

Management

Aims

To restore normal calcium and phosphorus in the body
To prevent further complications or disease progress

Admission

The child is admitted to pediatric ward in case the child is referred from outside the hospital.

Assessment

A demographic data of patient is taken which includes name, age, sex, etc
A detailed medical and obstetric history,prenata and natal data,birth weight, APGAR score at birth history are taken
Physical examination is done from head to toe putting more emphasis on bone formation to notify any abnormalities.

Immediate care

Baby is put in a comfortable, warm bed to prevent hypothermia.
Analgesics like paracetamol 2.5mg 8hourly for three days are administered to relieve pain which may be due to unknown fractures.
In case of fractures immobilisation is done which helps to maintain the bone in position.
Meanwhile the doctor is called who will come and perform a quick assessment and order for investigastions which will help him make a diagnosis depending on the results.

Investigations will include:

Blood to detect calcium and phosphorus levels and a protein called alkaline phosphate.
Ultra sound to rule out fractures.
X-rays to rule out the extent of fractures.

TREATMENT

The following treatment is administered to the patient as prescribed by the doctor.
Calcium 1.25mmol/kg /dose added to iv fluids like normal saline and ringers lactate given until the condition is stable.
Iv Phosphorus 1mmol/kg/dose added to iv fluids until the condition stabilizes.
Vitamin D supplements are given to children with liver problems.

Nursing interventions

Ensure the baby is warm and comfortable.
Monitoring of vital observations i.e. TPR
Ensure the patient is getting a diet rich in calcium and phosphorus. By feeding the baby with fortified milk
Physical exercises by the physiotherapists are encouraged
Ensure the baby is getting adequate rest and sleep by providing a conducive environment.
Psychological care is done to the mother to allay the anxiety
Both environmental and personal hygiene is promoted to prevent cross infection.
Administration of medicine to the patient as prescribed by the doctor.
Weekly monitoring of urine calcium, phosphorus.
When the patient improves discharge is considered.

Advise on discharge

Mother is advised to continue feeding the baby on a diet containing calcium and phosphorus.
Mother is also advised to handle the baby gently since there is a risk of broken bones.
A return date is given to help in the follow up and to know the prognosis of the disease

Osteopenia of Prematurity Read More »

$fractures$

Fractures

Fractures are complete or incomplete disruption in the continuity of the bone.
A fracture is a break in the continuity of a bone tissue, when subjected to excessive abnormal force or
A fracture is a break in the bone that occurs when more force is applied to the bone than the bone can withstand.
Fractures are also known as broken bones.

Common Childhood Fractures.

Arm bones are fractured more often than other bones.
Collarbone or shoulder fractures
Elbow fractures
forearm, wrist, or hand fracture
Leg, foot, or ankle fracture.

Causes of Fractures

Direct Force: in which the fracture occurs at the point of contact.
Torsion: in which the fracture occurs at the point opposite the location of the force, e.g. twisting of the foot may lead to break of bones of the leg.
Violent Contractions: e.g. forcibly throwing an object produces powerful muscle contractions which can fracture the humerus. Also in strong contractions in tetanus.
Disease Processes: cause weakening of the bone structure; osteoporosis, malnutrition, bone tumors

Risks for fractures

Sporting accidents
Falls from heights
Bike and car accidents
Poor nutrition; a diet low in calcium

Associated events following fractures.

When a bone is broken adjacent structures are also affected, resulting in;

Soft tissue edema
Joint dislocation
Ruptured tendons
Severed nerves
Damaged blood vessels
Hemorrhage into the muscles & joints

Classification of Fractures

Fractures can be grouped into 4 categories; i.e

Communication with environment.
By Anatomical Site
By Pattern
Miscellaneous

COMMUNICATION WITH ENVIRONMENT

Open/compound fracture: fractured part is exposed to the external environment. These are fractures where the bone is exposed through the skin or mucous membrane.
Closed/simple fracture: fracture with the overlying skin intact. These are types of fractures that do not penetrate the skin.
Complete fracture/Incomplete: Foe complete, the fracture line runs entirely through the bone substance with the periosteum disrupted on both sides of the bone and 2 fragments are present on either side of the fracture line. In incomplete, the fracture doesn’t entirely destroy the continuity of the bone.

BY ANATOMICAL SITE.

Avulsion: A fracture occurring from pulling effects of ligaments and tendons.
Potts Fracture : Type of fracture that occurs at the ankle joint.
Colles fracture(distal radius fracture): a fracture that occurs at the wrist joint.

BY PATTERN

Transverse : where the fracture in the bone is broken perpendicular to its length i.e. right angle to the bone.
Oblique: where the fracture extends in an oblique direction.
Spiral: fracture in which the born has been twisted apart.

MISCELLANEOUS

Green stick fracture: common in children and bone commonly bends or in severe cases, fracture line extends only half way across the bone substance. One side of the bone is broken, causing the other side to bend. A greenstick fracture resembles a broken tree branch. The branch cracks on one side but remains partially intact on the other.
Depressed fracture: a fracture having its edges driven below the surrounding bone surfaces, e.g. fractured skull.
Comminuted fracture: bone fragments are crushed or broken into small pieces. Occurs after high impact trauma eg a vehical road crash.
Displaced/overriding fracture: the bone fragments are separated away from the fracture line and bone ends are overlapping each other.
Impacted: where a bone fragment is moved into another.
Complicated fracture: that which is associated with many structures destroyed such as nerves, blood vessels, joints, muscles
Stress fracture: occurs on a normal or abnormal bone from constant exposure to stress e.g. running a long distance, jumping a rope
Pathological fracture: a fracture caused by a disease e.g bone cysts, paget’s disease.

Signs and symptoms of fractures

Pain at the site of injury : which is continuous and increases in severity until the bone fragments are immobilized.
Local tenderness.
Deformity : displacements, rotation of fragments in the fracture of the limb causes deformity(either palpable/visible). Is detectable when limb is compared with the uninjured extremity.
Soft tissue swelling
Loss of function : after the fracture, the extremity cannot function properly because normal function of muscles depends on the integrity of the bones to which they are attached.
Bruising
Involuntary muscle spasms.
Intense pain e.g. in the rib cage when a patient takes a deep breath or coughs.
Abnormal mobility
Involuntary muscle spasms
Crepitus – when the extremity is examined with the hands, a grating sound or sensation is heard or felt when broken ends rub on each other and is called crepitus.
Bone may be visibly seen protruding through the skin.
Impaired sensation/numbness may occur if there is nervous damage
Shock results from blood loss
Swelling and discoloration: localized swelling and discoloration of the skin (Ecchymosis) occurs after a fracture, as a result of trauma and bleeding into the tissues.

Assessment and Diagnostic Findings

To determine the presence of fracture, the following diagnostic tools are used.

History taking.
Physical Examinations.
X-ray examinations: Determines location and extent of fracture.
Bone scans, computed tomography (CT)/magnetic resonance imaging (MRI) scans: Visualizes fractures, bleeding, and soft-tissue damage.

Process of Fracture Healing

This process varies according to the type of bone involved type of fracture and the amount of movement at the fracture site. In the absence of rigid fixation in tubular bones, healing proceeds in five stages as follows;

1.Tissue destruction & haematoma formation:

After tissue destruction, torn blood vessels result to hematoma formation (which is a collection of clotted blood between the ends of the bones and in surrounding soft tissues. Fibrin, red blood cells, debris and inflammatory exudates come together and form a fibrin clot.

2.Inflammation & cellular proliferation:

This follows development of acute inflammation and accumulation of inflammatory exudate containing macrophages that phagocytose the hematoma and small fragments of bone without blood supply and this takes about 5 days. Fibroblasts migrate to the site, granulation tissue and new capillaries develop.

3. Stage of Callus formation (Soft Callus)

New bone forms as large number of osteoblasts secrete spongy bone, which unites the broken ends, osteoclasts begin mopping up the dead bone. The new deposits of bone and cartilage are called callus. As the immature bone (soft callus) becomes more densely mineralized, movement of the site progressively decreases.

4.Stage of consolidation(Hard callus)

Over the next few days, callus matures and the cartilage is gradually replaced with new bone.

5.Stage of remodelling

This is the reshaping of the callus by a continuous process of resorption and laydown. Internal callus is hollowed out into marrow cavity, while external callus is slowly removed. Reshaping of the bone continues and gradually the medullary canal is reopened through the callus, and callus tissue is completely replaced with mature compact bone. Often the bone is thicker and stronger at the repair site than originally and a second fracture is more likely to occur at a different site.

Healing of Fractures

Factors necessary for bone healing

Haematoma formation.
Contact of bone end and no interposition of other tissues
Continued immobilization until calus is able to withstand stress.
Good supply of blood
Enough rest of the fractured site
Good nutrition- calcium, proteins

Factors influencing bone healing.

(a). Systemic factors

-Age ( healing is almost twice as fast in children as in adults )
-Activity level.( immobilization)
-Nutritional status.
-Hormonal factors (GH, corticosteroids )
-Diseases e.g. DM, anaemia, neuropathies
-Vitamin deficiencies e.g. A C D K
-Drugs e.g. anti coagulants, anti inflammatory.

(b). Local factors.

-type of bone( cancellous heals faster than cortical bone)
-type of fracture. Spiral better than transverse.
-blood supply ( poor circulation-poor healing.)
-reduction- faster when there’s perfect reduction.
-infection
-soft tissue interposition
-mobilization. Early vs late mobilization.

Management

Aims of management.

To regain and maintain the normal alignment of the injured part.
To regain normal function of the injured part.
To achieve the above objectives for the patient in the shortest time possible

Basic principles of managing fractures

The principles of fracture management are:

Reduction
Immobilization
Rehabilitation

(1) Reduction: Reduction is the process of restoring the bone ends (and any fractured fragments) into their normal anatomical positions. This is accomplished by open or closed manipulation of the affected area, referred to as open reduction and closed reduction.

Closed reduction is accomplished by bringing the bone ends into alignment by manipulation and manual traction. X-rays are taken to determine the position of the bones. A cast is normally applied to immobilize the extremity and maintain the reduction.
In open reduction, a surgical opening is made, allowing the bones to be reduced manually under direct visualization. Frequently, internal fixation devices will be used to maintain the bone fragments in reduction.

(2) Immobilization: Immobilization is necessary to maintain fracture reduction until healing occurs. Immobilization may be accomplished by external or internal fixation.

Methods of external fixation include casts, splints, and continuous traction.
Internal fixation devices include pins, wires, screws, rods, nails, and plates.

(3) Rehabilitation: Rehabilitation is the regaining of strength and normal function in the affected area. Specific rehabilitation for each patient will be based upon the type of fracture and the methods of reduction and immobilization used.

First aid management

This can save the client’s life so it is crucial. A B C D of life criteria is used as follows;

Ensure that the patient is breathing then do the following:

Airway should be clear
Breathing should be maintained.
Check pulse and control bleeding.
Deformity should immobilized, Immobilize the limb to avoid more harm and pain by using splints.

Emergency Management of Fractures

Immediately after injury, whenever a fracture is suspected, it is important to immobilize the body part before the patient is moved.
If an injured patient must be removed from a vehicle before splints can be applied, the extremity is supported above and below the fracture site to prevent rotation as well as angular motion.
Adequate splinting, including joints adjacent to the fracture, is essential.
Movement of fracture fragments causes additional pain, soft tissue damage, and bleeding.
Temporary, well-padded splints, firmly bandaged over clothing, serve to immobilize the fracture.
Immobilization of the long bones of the lower extremities may be accomplished by bandaging the legs together, with the unaffected extremity serving as a splint for the injured one.
In an upper extremity injury, the arm may be bandaged to the chest, or an injured forearm may be placed in a sling.
The neurovascular status distal to the injury should be assessed to determine adequacy of peripheral tissue perfusion and nerve function.
With an open fracture, the wound is covered with a clean (sterile) dressing to prevent contamination of deeper tissues.
No attempt is made to reduce the fracture, even if one of the bone fragments is protruding through the wound.
Splints are applied for immobilization.
In the emergency department, the patient is evaluated completely.
The clothes are gently removed, first from the uninjured side of the body and then from the injured side.
The patient’s clothing may be cut away. The fractured extremity is moved as little as possible to avoid more damage

Management in hospital

Care depends on class/type of fracture
Immobilization/ reduction and rehabilitation is done.
Pain relief
Anti biotics
Supportive treatment eg feso4,FA ,multivitamin
Bone x- ray
Fluid resuscitation
Infection prevention
Nutrition – calcium
Exercises/ physiotherapy
Nursing care

Nursing Care

Encourage patients with closed (simple) fractures to return to their usual activities as rapidly as possible.
Teach patients how to control swelling and pain associated with the fracture and with soft tissue trauma and encourages them to be active within the limits of the fracture immobilization.
It is important to teach exercises to maintain the health of unaffected muscles and to increase the strength of muscles needed for transferring and for using assistive devices (eg, crutches, walker, special utensils).
Teach patients to use assistive devices safely. Plans are made to help patients modify their home environment as needed and to secure personal assistance if necessary.
Patient teaching include self-care, medication information, monitoring for potential complications and the need for continuing health care supervision.
Flracture healing and restoration of full strength and mobility may take months

Managing Fractures at Specific Sites

Maximum functional recovery is the goal of management.

Clavicle

Fracture of the clavicle (collar bone) is a common injury that results from a fall or a direct blow to the shoulder.
Monitor the circulation and nerve function of the affected arm and compare with the unaffected arm to determine variations, which may indicate disturbances in neurovascular status.
Caution the patient not to elevate the arm above shoulder level until the fracture has healed (about 6 weeks).
Encourage the patient to exercise the elbow, wrist, and fingers as soon as possible and, when prescribed, to perform shoulder exercises.
Tell the patient that vigorous activity is limited for 3 months.

Humeral Neck

With humeral neck fractures (seen most frequently in older women after a fall on an outstretched arm), perform neurovascular assessment of the involved extremity to evaluate the extent of injury and possible involvement of the nerves and blood vessels of the arm.
Teach the patient to support the arm and immobilize it by a sling and swathe that secure the supported arm to the trunk.
Begin pendulum exercises as soon as tolerated by the patient. Instruct the patient to avoid vigorous activity for an additional 10 to 14 weeks.
Inform the patient that residual stiffness, aching, and some limitation of range of motion may persist for 6 or more months.
When a humeral neck fracture is displaced with required fixation, exercises are started only after a prescribed period of immobilization.

Humeral shaft fractures

The nerves and brachial blood vessels may be injured, so neurovascular assessment is essential to monitor the status of the nerve or blood vessels.
Use well-padded splints to initially immobilize the upper arm and to support the arm in 90 degrees of flexion at the elbow, use a sling or collar and cuff to support the forearm, and use external fixators to treat open fractures of the humeral shaft.
Functional bracing may also be used for these fractures.
Teach patient to perform pendulum shoulder exercises and isometric exercises as prescribed.

Elbow

Elbow fractures (distal humerus) may result in injury to the median, radial, or ulnar nerves.
Evaluate the patient for paresthesia and signs of compromised circulation in the forearm and hand.
Monitor closely for Volkmann’s ischemic contracture (an acute compartment syndrome) as well as for hemarthrosis (blood in the joint).
Reinforce information regarding reduction and fixation of the fracture and planned active motion when swelling has subsided and healing has begun.
Explain care if the arm is immobilized in a cast or posterior splint with a sling. Encourage active finger exercises.
Teach and encourage patient to do gentle range of motion exercise of the injured joint about 1 week after internal fixation.

Radial head fractures

They are usually produced by a fall on the outstretched hand with the elbow extended.
Instruct patient in use of a splint for immobilization.
If the fracture is displaced, reinforce the need for postoperative immobilization of the arm in a posterior plaster splint and sling.
Encourage the patient to carry out a program of active motion of the elbow and forearm when prescribed

Wrist

Wrist fractures (distal radius [Colles’ fracture]) usually result from a fall on an open, dorsiflexed hand.
They are frequently seen in elderly women with osteoporotic bones and weak soft tissues that do not dissipate the energy of a fall.
Reinforce care of the cast, or with more severe fractures with wire insertion, teach incision care.
Instruct patient to keep the wrist and forearm elevated for 48 hours after reduction.
Begin active motion of the fingers and shoulder promptly by teaching patient to do the following exercises to reduce swelling and prevent stiffness:
Hold the hand at the level of the heart. Move the fingers from full extension to flexion. Hold and release. Repeat at least 10 times every hour when awake.
Use the hand in functional activities.
Actively exercise the shoulder and elbow, including complete range-of-motion exercises of both joints
Assess the sensory function of the median nerve by pricking the distal aspect of the index finger, and assess the motor function by testing patient’s ability to touch the thumb tot he little finger.
If diminished circulation and nerve function is noted, treat promptly.

Hand and Fingers

Hand trauma often requires extensive reconstructive surgery.
The objective of treatment is always to regain maximum function of the hand.
With a non displaced fracture, the finger is splinted for 3 to 4 weeks to relieve pain and protect the fingertip from further trauma, but displaced fractures and open fractures may require open reduction with internal fixation, using wires or pins.
Encourage functional use of the uninvolved portions of the hand
Evaluate the neurovascular status of the injured hand.
Teach the patient to control swelling by elevating the hand.

Pelvis

Pelvic fractures may be caused by falls, motor vehicle crashes, or crush injuries. At least two thirds of these patients have significant and multiple injuries.
Monitor for symptoms, including ecchymosis; tenderness over the symphysis pubis, anterior iliac spines, iliac crest, sacrum, or coccyx; local edema; numbness or tingling of the pubis, genitals, and proximal thighs; and inability to bear weight without discomfort.
Complete a neurovascular assessment of the lower extremities to detect injury to pelvic blood vessels and nerves.
As pain resolves, instruct patient to resume activity gradually, using assistive mobility devices for protected weight bearing. Patients with unstable pelvic fractures may be treated with external fixation or open reduction and internal fixation (ORIF).
Promote hemodynamic stability and comfort, and encourage early mobilization.
Examine urine for blood to assess for urinary tract injury. In male patients, do not insert a catheter until the status of the urethra is known.
Monitor for diffuse and intense abdominal pain, hyperactive or absent bowel sounds, and abdominal rigidity and resonance (free air) or dullness to percussion (blood), which suggest injury to the intestines or abdominal bleeding.
Monitor for hemorrhage and shock, two of the most serious consequences that may occur. Palpate both lower extremities for absence of peripheral pulses, which may indicate a torn iliac artery or one of its branches.
Assess for injuries to the bladder, rectum, intestines, other abdominal organs, and pelvic vessels and nerves.
If patient has a stable pelvic fracture, maintain patient on bed rest for a few days and provide symptom management until the pain and discomfort are controlled.
Provide fluids, dietary fiber, ankle and leg exercises, antiembolism stockings to aid venous return, logrolling, deep breathing, and skin care to reduce the risk for complications and to increase comfort.
Monitor bowel sounds. If patient has a fracture of the coccyx and experiences pain on sitting and with defecation, assist with sitz baths as prescribed to relieve pain, and administer stool softeners to prevent the need to strain on defecation.

Femur and Hip

Femoral shaft fractures are most often seen in young adults involved in a motor vehicle crash or a fall from a high place.
Frequently, these patients have associated multiple trauma and develop shock from a loss of 2 to 3 units of blood.
Assess neurovascular status of the extremity, especially circulatory perfusion of the lower leg and foot (popliteal, posterior tibial, and pedal pulses and toe capillary refill time as well as Doppler ultrasound monitoring).
Note signs of dislocation of the hip and knee, and knee effusion, which may suggest ligament damage and possible instability of the knee joint
Apply and maintain skeletal traction or splint to achieve muscle relaxation and alignment of the fracture fragments before ORIF procedures, and later a cast brace.
Assist patient in minimal partial weight bearing when indicated and progress to full weight bearing as tolerated.
Reinforce that the cast brace is worn for 12 to 14 weeks
Instruct in and encourage patient to perform exercises of lower leg, foot, and toes on a regular basis.
Assist patient in performing active and passive knee exercises as soon as possible, depending on the management approach and the stability of the fracture and knee ligaments.

Tibia and Fibula

Tibia and fibula fractures (most common fractures below the knee) tend to result from a direct blow, falls with the foot in a flexed position, or a violent twisting motion.
Provide instruction on care of the long leg walking cast or patellar-tendon-bearing cast.
Instruct patient in and assist with partial weight bearing,
usually in 7 to 10 days.
Instruct patient on care of a short leg cast or brace (in 3 to 4 weeks), which allows for knee motion.
Instruct patient in care of skeletal traction, if applicable.
Encourage patient to perform hip, foot, and knee exercises within the limits of the immobilizing device.
Instruct patient to begin weight bearing when prescribed (usually in about 4 to 8 weeks).
Instruct patient to elevate extremity to control edema.
Perform continuous neurovascular evaluation.

Rib

Rib fractures occur frequently in adults and usually result in no impairment of function but produce painful respirations.
Assist patient to cough and take deep breaths by splinting the chest with hands or pillow during cough.
Reassure patient that pain associated with rib fracture diminishes significantly in 3 or 4 days, and the fracture heals within 6 weeks.
Monitor for complications, which may include atelectasis, pneumonia, a flail chest, pneumothorax, and hemothorax.

COMPLICATIONS OF FRACTURES

Early complications include;

Shock,
Fat embolism,
Compartment syndrome, and
Venous thromboembolism (deep vein thrombosis [DVT],
Pulmonary embolism [PE]).

Delayed Complications;

Delayed union,
Malunion,
Nonunion,
Avascular necrosis (AVN) of bone, reaction to internal fixation devices
Complex regional pain syndrome (CRPS, formerly called reflex sympathetic dystrophy (RSD), is chronic condition of severe burning pain affecting one of the extremities
Heterotopic ossification- is the presence of bone in the soft tissue where bone normally does not exist

MANIFESTATION OF COMPLICATIONS

Fat embolism syndrome:

Occurs with blockage of the small blood vessels that supply the brain, lungs, kidneys, and other organs.
Sudden onset, usually occurring within 12 to 48 hour but may occur up to 10 days after injury),
Signs & symptoms: hypoxia, tachypnea, tachycardia, and pyrexia; dyspnea, crackles, wheezes, precordial chest pain, cough, large amounts of thick white sputum.

Compartment syndrome

Acute compartment syndrome may produce deep, throbbing, unrelenting pain not controlled by opioids
It can be due to a tight cast or constrictive dressing or an increase in muscle compartment contents because of edema or hemorrhage.
Signs & symptoms include; Cyanotic (blue-tinged) nail beds and pale or dusky and cold fingers or toes are present; nail bed capillary refill times are prolonged (greater than 3 seconds); pulse may be diminished or absent; and motor weakness, paralysis, and paresthesia may occur.

DIC- disseminated intravascular coagulation is evidenced by;

Unexpected bleeding after surgery and
Bleeding from the mucous membranes,
Venipuncture sites, and
Gastrointestinal and urinary tracts.

Infection. symptoms include.

Tenderness on examination
Pain (patient history)
Redness,
Swelling,
Local warmth,
Elevated temperature, and
Purulent drainage.

Nonunion is manifested by

Persistent discomfort and abnormal movement at the fracture site.

Some risk factors include;

Infection at the fracture site
Interposition of tissue between the bone ends
Inadequate immobilization or manipulation that disrupts callus formation,

MANAGEMENT OF COMPLICATIONS

Treatment of shock :

Consists of stabilizing the fracture to prevent further hemorrhage
Restoring blood volume and circulation
Relieving the patient’s pain
Providing proper immobilization and
Protecting the patient from further injury and other complications.

Prevention and management of fat embolism:

Include immediate immobilization of fractures
Adequate support for fractured bones during turning and positioning
Maintenance of fluid and electrolyte balance
Prompt initiation of respiratory support with prevention of respiratory and metabolic acidosis
Corticosteroids as well as vasopressor medications may be given.

Compartment syndrome:

Is managed by controlling swelling by elevating the extremity to heart level or by releasing restrictive devices (dressings or cast).
A fasciotomy (surgical decompression with excision of the fascia) may be needed to relieve the constrictive muscle fascia.
The wound remains open and covered with moist sterile saline dressings for 3 to 5 days.
The limb is splinted and elevated.
Prescribed passive range-of-motion exercises may be performed every 4 to 6 hours.

Nonunion (failure of the ends of a fractured bone to unite)

Is treated with internal fixation
Bone grafting
Electrical bone stimulation, or a combination of these.

Prevention and Control of HIV/AIDS

Prevention Framework in children and infants.

Prevention in Pediatrics

∙ Behavioral change and risk reduction interventions
∙ Biomedical prevention interventions
∙ Structural intervention

BEHAVIORAL CHANGE AND RISK REDUCTION INTERVENTIONS

The priority of behavioral interventions is to delay sexual debut; reduce unsafe sex and multiple, especially concurrent sexual partnerships; and discourage cross-generational and transactional sex.

Types of behavioral change

∙ Service delivery
∙ Risk assessment for client
∙ Provide socio-behavioral change Communication (SBCC) and link to services as appropriate ∙ Condom promotion and provision

Service delivery

The government of Uganda ensures that

1 . ⇒ Each health facility/program should have a focal person for HIV prevention

2. ⇒ All staff offering prevention services need to be trained

3. ⇒ Outreaches for key and priority populations

Risk assessment

4. ⇒ Offer HTS to sexually active adolescents, pregnant mothers who have not tested in the last 12 months or have had unprotected sex in last three months.

5. ⇒ HIV testing for infants born of HIV infected mothers.

6. ⇒ Assess sexual behavior of the in pregnant mothers and adolescents (ask if condoms are used, frequency, the number of partners, transactional sex/sex work) and if the client is involved in transactional sex/sex work encourage correct and consistent condom use.

Provide socio-behavioral change Communication (SBCC) and link to services as appropriate

7. ⇒ Discuss delay of onset of sexual debut in children and adolescents (abstinence) ⇒ Discuss correct and consistent condom use and offer condoms as appropriate to adolescents ⇒ Discourage multiple, concurrent sexual partnerships to promote faithfulness with a partner of known status.

8. ⇒ Discuss with the adolescents about sexual and reproductive health services and link to services as appropriate.

9. ⇒ Discourage risky cultural practices such as childhood marriages

10. ⇒ Identify, refer and link clients to other available facility and community programs

11. ⇒ Assess for violence, (physical, emotional, or sexual); if child discloses sexual violence, assess if the client was raped and act immediately

Condom promotion and provision

12. ⇒ Discuss condom use as an option for risk reduction in pregnant mothers and adolescent ∙ Discuss barriers to condom use to pregnant mothers and adolescent

13. ⇒ Clarify any questions and dispel myths around condoms

Biomedical prevention interventions

The key biomedical interventions include;

∙ EMTCT
∙ Safe male circumcision (SMC)
∙ ART
∙ PEP,
∙ PrEP
∙ Blood transfusion safety
∙ STI screening and treatment

Safe male circumcision (SMC)

Male circumcision is the surgical removal of the foreskin of the penis. SMC reduces the risk of HIV acquisition among circumcised men (adolescents) by approximately 60%.

Blood transfusion safety

Ensuring the screening of blood donors for HIV and hepatitis B
Ensuring proper storage and administration

STI screening and treatment

Integration of STI services in all health programs e.g. YCC, MCH.

EMTCT (Elimination of Mother-to-Child Transmission of HIV)

Measures of reducing the risk of HIV transmission to the child during pregnancy, labor, puerperium and breastfeeding.

Post-exposure prophylaxis (PEP)

Post-exposure prophylaxis (PEP) is the short-term use of ARVs to reduce the likelihood of acquiring HIV infection after potential occupational or non-occupational exposure.

Types of exposure:

∙ Occupational exposures occur in the health care or laboratory setting and include sharps and needlestick injuries or splashes of body fluids to the skin and mucous membranes.
Non-occupational exposures include unprotected sex, exposure following assault like in rape and defilement, and road traffic accidents.

Steps for providing Post Exposure Prophylaxis

Step 1: Clinical assessment and providing first aid

Conduct a rapid assessment of the client to assess exposure and risk and provide immediate care. Occupational exposure:

After a needlestick or sharp injury

∙ Do not squeeze or rub the injury site
∙ Wash the site immediately with soap or mild disinfectant (chlorhexidine gluconate solution) ∙ Use antiseptic hand rub/gel if no running water
∙ Don’t use strong, irritating antiseptics (like bleach or iodine)

After a splash of blood or body fluids in contact with intact skin

∙ Wash the area immediately
∙ Use antiseptic hand rub/gel if no running water
∙ Don’t use strong, irritating antiseptics (like bleach or iodine)

Step 2: Eligibility assessment

Provide PEP when:

∙ Exposure occurred within the past 72 hours; and
∙ The exposed individual is not infected with HIV; and
∙ The ‘source’ is HIV-infected, has unknown HIV status or is high risk

Do not provide PEP when:

∙ The exposed individual is already HIV-positive
∙ The source is established to be HIV-negative
∙ Individual was exposed to bodily fluids that do not pose a significant risk (e.g. tears, non-blood stained saliva, urine, sweat)
∙ Exposed individual declines an HIV test

Step 3: Counseling and support

Counsel on:

∙ The risk of HIV from the exposure
∙ Risks and benefits of PEP
∙ Side effects of ARVs
∙ Enhanced adherence if PEP is prescribed
∙ Importance of linkage for further support for sexual assault cases

Step 4: Prescription

∙ PEP should be started as early as possible, not beyond 72 hours of exposure ∙ Recommended regimens include:

⇒ Pregnant mothers/adults: TDF+3TC+ATV/r
⇒ Children: ABC+3TC+LPV/r

∙ A complete course of PEP should run for 28 days

∙ Do not delay the first doses because of lack of baseline HIV test

∙ Document the event and patient management in the PEP register (ensure confidentiality of patient data)

Step 5: Provide follow-up

∙ Discontinue PEP after 28 days
∙ Perform follow-up HIV testing three months after exposure
∙ Counsel and link to HIV clinic for care and treatment if HIV-positive
∙ Provide prevention and education/risk reduction counseling if HIV-negative

ORAL PRE-EXPOSURE PROPHYLAXIS (PrEP)

PrEP is the use of ARV drugs by people who are not infected with HIV to block the acquisition of HIV.

The process of providing pre-exposure prophylaxis (PrEP)

∙ Eligibility for PrEP
∙ Screening for PrEP eligibility
∙ Steps to initiation of PrEP
∙ Follow-up/ monitoring clients on PrEP
∙ Guidance on discontinuing PrEP

Step 1: Eligibility for PrEP

PrEP provides an effective additional biomedical prevention option for HIV-negative people at substantial risk of acquiring HIV infection. These include people who:

∙ Have multiple sexual partners
∙ Engage in transactional sex including sex workers
∙ Use or abuse injectable drugs and alcohol
∙ Have had more than one episode of an STI within the last twelve months
∙ Are part of a discordant couple, especially if the HIV-positive partner is not on ART or has been on ART for less than six months
∙ Are recurrent users of PEP (3 consecutive cycles of PEP)
∙ Engage in anal sex

These risk factors are likely to be more prevalent in populations such as sex workers, fisher folk, long distance truck drivers, men who have sex with men (MSM), uniformed forces, and adolescents and young women engaged in transactional sex.

Step 2; Screening for PrEP eligibility

After meeting the eligibility criteria:

∙ Confirm HIV-negative status
∙ Rule out acute HIV infection
∙ Assess for hepatitis B infection: if negative, patient is eligible for PrEP; if positive, refer patient for management
∙ Assess for contraindications to TDF/FTC

Step 3: Steps to initiation of PrEP

Provide risk-reduction and PrEP medication adherence counseling:
∙ Provide condoms and education on their use
∙ Initiate a medication adherence plan
∙ Prescribe a once-daily pill of TDF (300mg) and FTC (200mg)
∙ Initially, provide a 1-month TDF/FTC prescription (1 tablet orally, daily) together with a 1-month follow-up date
∙ Counsel client on side effects of TDF/FTC

Step 4: Follow-up/ monitoring clients on PrEP

∙ After the initial visit, the patient should be given a two-month follow-up appointment and thereafter quarterly appointments
∙ Perform an HIV antibody test every three months
∙ For women, perform a pregnancy test based on clinical history
∙ Review the patient’s understanding of PrEP, any barriers to adherence, tolerance to the medication as well as any side effects
∙ Review the patient’s risk exposure profile and perform risk-reduction counseling ∙ Evaluate and support PrEP adherence at each clinic visit
∙ Evaluate the patient for any symptoms of STIs at every visit and treat as needed

Step 5: Guidance on discontinuing PrEP

∙ Acquisition of HIV infection
∙ Changed life situations resulting in lowered risk of HIV acquisition
∙ Intolerable toxicities and side effects
∙ Chronic non-adherence to the prescribed dosing regimen despite efforts to improve daily pill-taking ∙ Personal choice
∙ HIV-negative in a sero-discordant relationship when the positive partner has achieved sustained viral load suppression (condoms should still be used consistently.

MOTHER-TO-CHILD TRANSMISSION OF HIV

Approximately one-third of the women who are infected with HIV can pass it to their babies.

Elements of elimination of mother to child transmission

∙ : Primary prevention of HIV infection Women and men of reproductive age including adolescents
∙ : Prevention of unintended pregnancies among women living with HIV Women including adolescents living with HIV and their partners.
∙ : Prevention of HIV transmission from women living with HIV to their infants Pregnant and breastfeeding women including adolescents living with HIV
∙: Provision of treatment, care, and support to women infected with HIV, their children and their families Women living with HIV and their families

Cause

Time of transmission;

∙ During pregnancy (15-20%)
∙ During time of labour and delivery (60%-70%)
∙ After delivery through breast feeding (15%-20%)

Pre-disposing factors

∙ High maternal viral load
∙ Depleted maternal immunity (e.g. very low CD4 count)
∙ Prolonged rupture of membranes
∙ Intra-partum haemorrhage and invasive obstetrical procedures
∙ If delivering twins, first twin is at higher risk of infection than second twin
∙ Premature baby is at higher risk than term baby
∙ Mixed feeding carries a higher risk than exclusive breastfeeding or use of replacement feeding

Investigations

∙ Blood: HIV serological test
∙ HIV -DNA/ PCR testing of babies.

Management

All HIV services for pregnant mothers are offered in the MCH clinic. After delivery, mother and baby will remain in the MCH postnatal clinic till HIV status of the child is confirmed, then they will be transferred to the general ART clinic.

The current policy aims at elimination of Mother-to-Child Transmission (eMTCT) through provision of a continuum of care with the following elements:

∙ Primary HIV prevention for men, women and adolescents
∙ Prevention of unintended pregnancies among women living with HIV
∙ Prevention of HIV transmission from women living with HIV to their infants
∙ Provision of treatment, care and support to ALL women infected with HIV, their children and their families

Management of HIV Positive Pregnant Mother

Key Interventions for eMTCT ;

∙ Routine HIV Counseling and Testing during ANC (at 1st contact. If negative, repeat HIV test in the third trimester/ labour.
∙ Enrolment in HIV care if mother is positive and not yet on treatment
∙ If mother already on ART, perform viral load and continue current regimen
∙ ART in pregnancy, labour and post-partum, and for life – Option B+

Treatment

Recommended ARV for option B+

One daily Fixed Dose Combination (FDC) pill containing TDF + 3TC + EFV started early in pregnancy irrespective of the CD4 cell count and continue during labour and delivery, and for life, Alternative regimen for women who may not tolerate the recommended option are: ∙
If TDF contraindicated: ABC+3TC+EFV
If EFV contraindicated: TDF + 3TC + ATV/r

Prophylaxis for opportunistic infections

Cotrimoxazole 960 mg 1 tab daily during pregnancy and postpartum

NB. Mothers on cotrimoxazole DO NOT NEED IPTp with SP for malaria

Notes

∙ TDF and EFV are safe to use in pregnancy
∙ Those newly diagnosed during labour will begin HAART for life after delivery

Caution

∙ In case of low body weight, high creatinine, diabetes, hypertension, chronic renal disease, and concomitant nephrotoxic medications: perform renal function investigations before starting TDF ∙ TDF is contraindicated in advanced chronic renal disease.

Prevention and Control of HIV/AIDS Read More »

Treatment of HIV/AIDS in Children (ARV therapy)

hiv / aids Treatment in Children

Treatment Modalities of HIV/AIDS

Treatment Modality	Description
Antiretroviral Therapy (ART)	Suppresses viral load to undetectable levels, reducing morbidity, mortality, and transmission of HIV.
Treatment of Acute Bacterial Infections	Addresses immediate bacterial infections.
Prophylaxis and Treatment of Opportunistic Infections	Prevents and manages opportunistic infections.
Maintenance of Good Nutrition	Ensures adequate nutrition to support overall health.
Immunization	Administers vaccines to prevent opportunistic infections.
Management of AIDS-Defining Illnesses	Addresses specific illnesses associated with advanced HIV infection.
Psychological Support for the Family	Provides emotional support and guidance for affected families.
Palliative Care for the Terminally Ill	Offers comfort and support for patients nearing the end of life.

ANTIRETROVIRAL DRUG TREATMENT

The goal of ART

Goal of ART: Suppress viral load to undetectable levels, reducing morbidity, mortality, and transmission of HIV.

When to Initiate ARV:

All HIV-infected children below 12 months.
Clinical AIDS
Mild to moderate symptoms and immunosuppression.

Process of Starting ART:

Assess all clients for opportunistic infections especially TB and cryptococcal meningitis. If the patient has TB or cryptococcal meningitis, ART should be deferred and initiated after starting treatment for these OIs. Treatment for other OIs and ART can be initiated concurrently.
For patients without TB or cryptococcal meningitis, offer ART on the same day through an opt-out approach. In this approach, the patients should be prepared for ART on the same day and assessed for readiness to start ART using the readiness checklist
If a client is ready, ART should be initiated on the same day. If a client is not ready or opts out of same-day initiation, a timely ART preparation plan should be agreed upon with the aim of initiating ART within seven days for children and pregnant women, and within one month for adults.

Principles for selecting the ARV regimens

The first-line ART regimens for treating HIV infection in Uganda were selected based on the following principles:

∙ Regimen with lower toxicity
∙ Better palatability and lower pill burden
∙ Increased durability and efficacy
∙ Sequencing: spares other available formulations for use in the 2nd line regimen ∙ Harmonization of regimen across age and population
∙ Lower cost
∙ Help the country to achieve a recommended regimen for the vast majority of PLHIV(People Living With HIV)

Available ARVs in Uganda

Drug Class	Examples
Nucleoside Reverse Transcriptase Inhibitors (NRTIs): Incorporate into the DNA of the virus, thereby stopping the building process.	Tenofovir (TDF), Zidovudine (AZT), Lamivudine (3TC), Abacavir (ABC)
Non-Nucleoside Reverse Transcriptase Inhibitors (NNRTIs): stop HIV production by binding directly onto the reverse transcriptase enzyme, and prevent the conversion of RNA to DNA.	Efavirenz (EFV), Nevirapine (NVP), Etravirine (ETV)
Integrase Inhibitors: interfere with the HIV DNA’s ability to insert itself into the host DNA and copy itself.	Dolutegravir (DTG), Raltegravir (RAL)
Protease Inhibitors (PIs): prevent HIV from being successfully assembled and released from the infected CD4 cell.	Atazanavir (ATV), Lopinavir (LPV), Darunavir (DRV)
Entry Inhibitors: prevent the HIV virus particle from infecting the CD4 cell.	Enfuvirtide (T-20), Maraviroc

Uses of ART (Antiretroviral Therapy)

Treatment of HIV/AIDS: ART is the primary treatment for managing HIV/AIDS, helping to control the viral load and maintain the health of the immune system.
Prevention of Mother-to-Child Transmission (PMTCT): ART is crucial in preventing the transmission of HIV from an infected mother to her baby during pregnancy, childbirth, and breastfeeding.
Post-Exposure Prophylaxis (PEP): ART is used as an emergency intervention for individuals who have been potentially exposed to HIV. It must be started within 72 hours of exposure to be effective.
Pre-Exposure Prophylaxis (PrEP): ART can be taken by HIV-negative individuals at high risk of infection to prevent acquiring HIV. This is particularly useful for people with HIV-positive partners, among others.
Treatment and Support for Children: Ensuring children with HIV receive ART is essential for their growth, development, and long-term health. Adherence to the treatment regimen is crucial for its effectiveness.
Reducing Viral Load to Undetectable Levels: ART helps reduce the viral load in the body to undetectable levels, significantly lowering the risk of HIV transmission and improving overall health.
Improving Quality of Life: Effective ART can improve the quality of life for people living with HIV by reducing the incidence of opportunistic infections and other HIV-related complications.
Increasing Life Expectancy: ART has been shown to increase the life expectancy of people living with HIV, allowing them to live longer, healthier lives.
Preventing Sexual Transmission of HIV: By reducing the viral load to undetectable levels, ART can prevent the sexual transmission of HIV, a strategy known as “treatment as prevention” (TasP).
Reducing HIV-Related Stigma and Discrimination: Successful ART can help reduce stigma and discrimination associated with HIV by enabling individuals to lead healthy, productive lives, thereby changing perceptions about the disease.
Managing Co-Infections: ART can help in managing co-infections such as hepatitis B and C, tuberculosis, and other conditions that are common in people living with HIV.

Recommended First Line Regimens in Adults, Adolescents, Pregnant Women and Children

HIV management guidelines are constantly being updated according to evidence and public policy decisions. Always refer to the latest official guidelines.

The 2022 guidelines recommend DOLUTEGRAVIR (DTG) an integrase inhibitor as the anchor ARV in the preferred first and second-line treatment regimens for all HIV infected clients; children, adolescents, men, women (including pregnant women, breastfeeding women, adolescent girls and women of child bearing potential).

Patient Category	Preferred Regimens	Alternative Regimens
Adults and Adolescents
Adults (including pregnant women, breastfeeding mothers, and adolescents ≥30Kg)	TDF + 3TC + DTG	– If DTG is contraindicated: TDF + 3TC + EFV400 – If TDF is contraindicated: TAF + FTC + DTG – If TDF or TAF is contraindicated: ABC + 3TC + DTG – If TDF or TAF and DTG are contraindicated: ABC + 3TC + EFV400 – If EFV and DTG are contraindicated: TDF + 3TC + ATV/r or ABC + 3TC + ATV/r
Children
Children ≥20Kg – <30Kg	ABC + 3TC + DTG	– If DTG is contraindicated: ABC + 3TC + LPV/r (tablets) – If ABC is contraindicated: TAF + FTC + DTG (for children >6 years and >25Kg) – If ABC and TAF are contraindicated: AZT + 3TC + DTG
Children <20Kg	ABC + 3TC + DTG	– If intolerant or appropriate DTG formulations are not available: ABC + 3TC + LPV/r granules – If intolerant to LPV/r: ABC + 3TC + EFV (in children >3 years and >10Kg) – If ABC is contraindicated: AZT + 3TC + DTG or LPV/r

Notes:

Contraindications for DTG include known diabetics, patients on anticonvulsants (carbamazepine, phenytoin, phenobarbital) – use the DTG screening tool prior to DTG initiation.
Contraindications for TDF and TAF include renal disease and/or GFR <60ml/min, weight <30Kg.
TAF can be used in subpopulations with bone density anomalies.
Children will be assessed individually for their ability to correctly take the different formulations of LPV.

Notes from Ministry of Health

For clients on an ABC-3TC-DTG based regimen weighing >25 kg, use the fixed-dose combination of Abacavir/Lamivudine/Dolutegravir 600/300/50 mg instead of the separate pills of Abacavir/Lamivudine 600/300 mg plus Dolutegravir 50 mg.
Use Abacavir/Lamivudine 600/300 mg for patients on the following regimens: ABC-3TC-ATV/r, ABC-3TC-LPV/r, and ABC-3TC-DRV/r.
Use the single pill of Dolutegravir 50 mg for patients on AZT-3TC-DTG based regimens.
For eligible patients on ATV/r and LPV/r, optimize to Dolutegravir.
For PrEP, while the guidelines provide options for the use of either TDF/3TC 300/300 mg or TDF/FTC 300/200 mg, use TDF/FTC 300/200 mg for PrEP in terms of programmatic implementation.

RECOMMENDED FIRST-LINE REGIMEN FOR INITIATION OF ART IN CHILDREN UNDER 3 YEARS OF AGE

Recommended first-line regimen: ABC+3TC+LPV/r

All HIV-infected children under 3 years should be initiated on abacavir + lamivudine + ritonavir-boosted lopinavir (ABC+3TC+LPV/r).

NB: Children younger than 36 months have a reduced risk of discontinuing treatment, viral failure or death if they start on an LPV/r based regimen instead of the NVP-based regimen. Also, surveillance of drug resistance among vertically infected children younger than 18 months in

Uganda has revealed high levels of resistance to NNRTIs and LPV/r is known to have a high barrier to resistance.

When to use alternative first-line regimens AZT+3TC+LPV/r

AZT+3TC+ LPV/r should only be used in children who experience a hypersensitivity reaction to abacavir (ABC), however, this is rare in African populations.

WHAT REGIMEN TO SWITCH TO (SECOND-LINE AND THIRD-LINE ART)

Second-line ARVS in adolescents/children above 10 years

Recommended 2nd line regimen: 2 NRTIs +ATV/r

HIV-infected adolescents/children above 10 years, initiating 2nd line ART should be initiated on 2 NRTIs and ritonavir-boosted atazanavir (ATV/r). The choice of NRTI should be determined based on the regimen the patient was on.

The recommended sequence is:

After failing on TDF + 3TC or ABC+3TC based regimen, use AZT+3TC
After failing on AZT+3TC based regimen, use TDF + 3TC

When to use alternative 2nd line regimen: 2 NRTIs +LPV/r

LPV/r is should only be used to initiate adolescents/children who weigh less than 40kg.

Second-line ARVS in children aged 3 years to less than 10 years

RECOMMENDED 2nd line REGIMEN: 2 NRTIs +LPV/r

HIV-infected children aged 3 to less than 10 years initiating 2nd line ART should be initiated on 2 NRTIs and ritonavir-boosted lopinavir (LPV/r). The recommended formulation is the LPV/r 100/25mg tablet. The choice of NRTI should be determined based on the regimen the patient was on The recommended sequence of the NRTIs is below:

∙ After failing on ABC+3TC based regimen, use AZT+3TC.

∙ After failing on AZT+3TC based regimen, used ABC+3TC.

Second-line ARVS in children under 3 years

Recommended 2nd line regimen: 2 NRTIs +RAL

HIV-infected children less than 3 years of age initiating 2nd line ART should be initiated on 2 NRTIs and RAL. The choice of NRTI should be determined based on the regimen the patient was on (Table 55). The recommended sequence of the NRTIs is:

∙ After failing on ABC+3TC based regimen, use AZT+3TC.

∙ After failing on AZT+3TC based regimen, used ABC+3TC.

The rationale for using raltegravir

Raltegravir is the recommended drug of choice for the second line ARVs in children with prior exposure to protease inhibitors because there is no data on safety and efficacy of dolutegravir in children under six years, while darunavir is contraindicated in this age group.

When to use alternative 2nd line regimen: 2 NRTIs + LPV/r

LPV/r is recommended in children who have used NNRTI (NVP) in their first line regimen.

Monitoring of ARV Treatment

The monitoring of patients on antiretroviral therapy (ART) serves several purposes:

Assess Response to ART and Diagnose Treatment Failure
Ensure Safety of Medicines: Identify Side Effects and Toxicity
Evaluate Adherence to ART

Methods of Monitoring ARV Treatment

1. Clinical Monitoring: Involves medical history and physical examination.

2. Laboratory Monitoring: Includes various laboratory tests.

Viral Load Monitoring: Preferred for assessing response to ART and diagnosing treatment failure.
CD4 Monitoring: Recommended in specific scenarios.
Other Minor Laboratory Tests: Includes tests for specific indications.

Viral Load Monitoring

Preferred method for monitoring ART response. A patient who has been on ART for more than 6 months and is responding to ART should have viral suppression (VL <1000 copies/ml) irrespective of the sample type (either DBS or plasma).
Provides an early and more accurate indication of treatment failure and the need to switch from first line to second-line drugs, hence reducing the accumulation of drug resistance mutations and improving clinical outcomes.
Early and accurate indication of treatment failure.
Differentiates between treatment failure and non-adherence.
Recommended frequency: Every six months for children and adolescents under 19 years.

CD4 Monitoring

Baseline CD4 count is essential for assessing opportunistic infection risk.
Recommended for patients with high viral load or advanced clinical disease.

Other Laboratory Tests

Tests	Indication
CrAg	Screen for cryptococcal infection
Complete Blood Count (CBC)	Assess anaemia risk
TB Tests	Suspected tuberculosis
Serum Creatinine	Assess kidney function
ALT, AST	Evaluate liver function
Lipid Profile, Blood Glucose	Assess metabolic health

Problems Associated with ARV Treatment

Immune Reconstitution Inflammatory Syndrome (IRIS)

IRIS is a spectrum of clinical signs and symptoms linked to immune recovery triggered by ART. It occurs in 10–30% of individuals starting ART, usually within the first 4–8 weeks.

Serious Forms: Most severe cases happen in patients co-infected with TB, Cryptococcus, Kaposi’s sarcoma, and herpes zoster.
Risk Factors: Include low CD4+ cell count (<50 cells/mm3) at ART initiation and disseminated opportunistic infections.
Management: Usually self-limiting; treat co-infections to reduce symptoms and reassure patients to maintain ART adherence.

Steps to Reduce IRIS Development

Early HIV Diagnosis: Initiate ART before CD4 declines to below 200 cells/mm3.
Optimal Management of Opportunistic Infections: Screen and treat infections before starting ART, especially TB and cryptococcus.

ARV Drug Toxicity

Range of Toxicities: ARVs can cause mild to life-threatening side effects.
Challenges: Differentiating between ARV toxicity and HIV complications can be complex.
Management: Assess patients for side effects at every clinic visit and take appropriate actions based on severity.

Management of ARV Side Effects/Toxicities

Category	Action
Severe, Life-threatening Reactions (e.g., SJS/TEN, severe hepatitis)	– Discontinue all ARVs immediately. – Manage the medical event and substitute offending drug when stable.
Severe Reactions (e.g., Hepatitis and Anemia)	– Substitute offending drug without stopping ART.
Moderate Reactions (e.g., Gynaecomastia, Lipodystrophy)	– Substitute with a drug in the same class or different class with a different toxicity profile. – Do not discontinue ART; continue if feasible.
Mild Reactions (e.g., Headache, Minor Rash, Nausea)	– Do not discontinue or substitute ART. – Provide reassurance and support to mitigate adverse reactions. – Counseling about the events.

Management of HIV Positive Pregnant Mother

Key Interventions for eMTCT:

Routine HIV Counseling and Testing during ANC (at 1st contact. If negative, repeat HIV test in the third trimester/ labour).
Enrolment in HIV care if the mother is positive and not yet on treatment.
If the mother is already on ART, perform viral load and continue the current regimen.
ART in pregnancy, labour, post-partum, and for life – Option B+.

Recommended ARV for option B+:

One daily Fixed Dose Combination (FDC) pill containing TDF + 3TC + EFV started early in pregnancy irrespective of the CD4 cell count and continued during labor and delivery, and for life.

Alternative regimens for women who may not tolerate the recommended option are:

If TDF contraindicated: ABC+3TC+EFV
If EFV contraindicated: TDF + 3TC + ATV/r
TDF and EFV are safe to use in pregnancy.
Those newly diagnosed during labor will begin HAART for life after delivery.

Prophylaxis for Opportunistic Infections

Cotrimoxazole 960 mg 1 tab daily during pregnancy and postpartum –– Mothers on cotrimoxazole DO NOT NEED IPTp with SP for malaria.

Care of HIV Exposed Infant

HIV-exposed infants should receive care at the mother-baby care point together with their mothers until they are 18 months old. A mother-baby care point is a healthcare facility that provides comprehensive services to both HIV-exposed infants and their parents.

The goals of HIV-exposed infant care services are:

To prevent the infant from being HIV infected.
Among those who get infected: to diagnose HIV infection early and treat it.
Offer child survival interventions to prevent early death from preventable childhood illnesses.

The HIV Exposed Infant and the mother should consistently visit the health facility at least nine times during that period i.e (i.e., at 6, 10 and 14 weeks, then at 5, 6, 9, 12, 15 and 18 months).

Nevirapine Prophylaxis

Provide NVP syrup from birth for 6 weeks: Give NVP for 12 weeks for babies at high risk, that is breastfeeding infants who mothers:

Have received ART for 4 weeks or less before delivery; or
Have VL >1000 copies in 4 weeks before delivery; or
Diagnosed with HIV during 3rd trimester or breastfeeding period (Postnatal)

Do PCR at 6 weeks (or at first encounter after this age) and start cotrimoxazole prophylaxis

If PCR positive, start treatment with ARVs and cotrimoxazole and repeat PCR (for confirmation)
If PCR negative and the baby never breastfed, the child is confirmed HIV negative. Stop cotrimoxazole, continue clinical monitoring and do HIV serology test at 18 months.
If PCR is negative but the baby has breastfed/is breast feeding, start/continue cotrimoxazole prophylaxis and repeat PCR 6 weeks after stopping breastfeeding.
Follow up any exposed child and do PCR if they develop any clinical symptom suggestive of HIV at any time and independently of previously negative results.
For negative infants, do serology at 18 months before final discharge.

Dosages of Nevirapine

Age Group	Weight Range	Dosage	Syrup Volume (10 mg/ml)
Child 0-6 weeks	2-2.5 Kg	10 mg once daily	1 ml
Child 0-6 weeks	>2.5 Kg	15 mg once daily	1.5 ml
Child 6 weeks – 12 weeks	Any weight	20 mg once daily	2 ml

Cotrimoxazole Prophylaxis: Provide cotrimoxazole prophylaxis to all HIV exposed infants from 6 weeks of age until they are proven to be uninfected.

Child <5 kg: 120 mg once daily
Child 5-14.9 kg: 240 mg once daily

Isoniazid (INH) Preventive Therapy (IPT):

Give INH for six months to HIV-exposed infants who are exposed to TB.
Isoniazid 10 mg/kg + pyridoxine 25 mg daily
For newborn infants, if the mother has TB disease and has been on anti-TB drugs for at least two weeks before delivery, INH prophylaxis is not required.

Immunization

Immunise HIV exposed children as per national immunisation schedule.

In case of missed BCG at birth, do not give if the child has symptomatic HIV.

Avoid yellow fever vaccine in symptomatic HIV.

Measles vaccine can be given even in symptomatic HIV.

Counselling on Infant Feeding Choice

Explain the risks of HIV transmission by breastfeeding (15%) and other risks of not breastfeeding (malnutrition, diarrhoea).
Mixed feeding may also increase the risk of HIV transmission and diarrhoea.
Tell her about options for feeding, advantages, and risks.
Help her to assess choices, decide on the best option, and then support her choice.

Feeding Options

Recommended option: Exclusive breastfeeding, then complementary feeding after the child is 6 months old.
Exclusive breastfeeding stopping at 3-6 months old if replacement feeding is possible after this.
If replacement feeding is introduced early, the mother must stop breastfeeding.
Replacement feeding with home-prepared formula or commercial formula and then family foods (provided this is acceptable, feasible, safe, and sustainable/affordable).

If Mother Chooses Breastfeeding

The risk may be reduced by keeping the breasts healthy (mastitis and cracked nipples raise HIV infection risk).
Advise exclusive breastfeeding for 3-6 months.

If Mother Chooses Replacement Feeding

Counsel and teach her on safe preparation, hygiene, amounts, times to feed the baby, etc.
Follow up within a week from birth and at any visit to the health facility.

hiv / aids Treatment in Children Read More »

Treatment of HIV/AIDS in Children (ARV therapy)

Treatment of HIV/AIDS begins after confirmation through the following diagnostic procedures.

Diagnostic Measures / Investigations.

Criteria for diagnosis of HIV/AIDS:

∙ Clinical Stage criteria
∙ HIV blood test must be positive

A reactive rapid test result must be confirmed before a diagnosis of infection can be given. Most commonly used to screen blood for donation in order to exclude those in the window period is ELISA AglAb tests

The test that Detects the genetic material of HIV itself (rather than antibodies or antigens) are known as PCR tests PCR (polymerase chain reaction) test is a type of test under Nucleic-acid Amplification testing (NAT).

NB: These tests should be used in conjunction with the clinical status, history, and risks factors of the person being tested.

HIV testing provision steps/protocol

∙ Pre-test information and counseling
∙ HIV testing
∙ Post-test counseling (individual/couple)
∙ Linkage to other services

Step 1: Pre-test information and counseling

Help the client/patient to know the ways HIV is transmitted and basic HIV preventive measures, benefits of HIV testing, possible test results and services available, consent and confidentiality, individual risk assessment, and fill the HTS card. Allow clients/patients to ask questions.

Step 2: HIV testing

Will be done using blood. For those below 18 months, a DNA PCR test will be done and those above 18 months an antibody test will be done. Refer to the HIV testing algorithms for the different age groups.

Step 3: Post-test counseling (individual/couple)

Assess readiness to receive results. Give results simply. Address concerns, disclosure, partner testing and risk reduction. Provide information about basic HIV care and ART care; complete the HTS card and HTS register.

Step 4: Linkage to other services

Provide information about services; fill the triplicate referral form. When the patient is enrolled, enter the pre-ART enrolment number into the HTS register and subsequently into the ART register when the patient is initiated on ART.

Principles of HIV testing services (HTS)

HTS delivery shall be non-discriminatory and offered using a human rights approach that observes the 5Cs (Confidentiality, Consent, Counseling, Correct test result and Connection to appropriate services). These principles are described below.

∙ Confidentiality: All providers should ensure privacy during HTS provision. All information discussed with clients should not be disclosed to another person without the client’s consent.

∙ Consent: All persons 12 years and above should consent to HTS on their own. In situations where consent cannot be obtained, the parent or guardian (of a child), next of kin, or legally authorized person should consent.

∙ Counseling: All persons accessing HTS should be provided with quality counseling before and after testing as per the approved HTS protocol.

∙ Correct test result: HTS providers should adhere to the national testing algorithm and must follow the Standard Operating Procedure for HIV testing to ensure that clients receive correct HIV test results.

∙ Connect to other services: Providers should link HTS clients to appropriate HIV prevention, treatment, care and support services.

Places to prick a child

∙ Infants age 1-4 months, less than 6kg heels work best
∙ Infants age 5-10 months, less than 10kg toes work best
∙ Larger infants and older children use the ring or middle finger

HIV testing algorithm for infants and children below 18 months of age

A virological test (DNA/PCR) is recommended for determining HIV status in infants and children below 18 months of age. The sample for testing should be collected using dried blood spot (DBS) specimens. The 1st DNA/PCR test should be done at six weeks of age or the earliest opportunity thereafter. Interpretation of the results and further testing are guided by the testing algorithm.

∙ A POSITIVE DNA/PCR test result indicates that the child is HIV-infected. All infants with a positive DNA/PCR test result should be initiated on ART and another blood sample should be collected on the day of ART initiation to confirm the positive DNA/PCR HIV test result.

∙ A NEGATIVE 1st DNA/PCR test result means that child is not infected, but could become infected if they are still breastfeeding. Infants testing HIV negative on DNA/PCR should be retested using DNA/PCR six weeks upon cessation of breastfeeding. Infants with 2nd negative DNA/PCR test should have a final rapid antibody test performed at 18 months.

Antibody tests can be used:

In children <18months of age to:

∙ Determine HIV- exposure in infants born to mothers of unknown HIV status
∙ Exclude infection in an infant at 18 months of age if the child has ceased breastfeeding for at least 6 weeks

∙ In Children > 18 months of age to confirm HIV infection

∙ HIV DNA PCR testing should be carried out on:
∙ Every HIV-exposed baby at 6 weeks of life or at first clinic visit if > 6weeks of age

Figure showing HIV testing algorithm for children <18 months of age

Procedure for DBS collection

Warm the area
Position baby with foot down
Sterilize area with alcohol
Allow to air dry
Press lancet into foot, prick skin
Wipe away first drop
Allow large drop to collect
Add 50ul (approx 2 drops) into one circle and fill it
Fill at least 3 circles
Clean foot, do not bandage
Dispose of all contaminated material appropriately

Figure showing serial HIV testing algorithm for persons above 18 months of age

Cautions during HIV testing

∙ Never use expired HIV test kits.
∙ Avoid modification of procedures
∙ Avoid use of clotted blood.
∙ Avoid use of ‘dirty’ blood (skin flakes, powder, sweat etc.)
∙ Avoid introducing air bubbles into the devices when adding the sample.

∙ Do not

⇒ Add more or less blood
⇒ Add more or less buffer
⇒ Exchange buffers
⇒ Contaminate the buffer
⇒ Modify the incubation time

LINKAGE FROM HIV TESTING TO HIV PREVENTION, CARE AND TREATMENT

Linkage refers to the process of connecting individuals who have tested positive for HIV from one service point to another.

Linkage to care is successful if the patient/client receives the services they have been referred to receive. For all clients who test HIV-positive, linkage should occur within seven days (within the same facility) and 30 days for inter-facility or community-to- facility referrals. It is recommended to use lay providers (community- and facility-based) as linkage facilitators. The process of linkage within the same health facility is described below

Types of linkages

∙ Internal facility linkage
∙ Inter facility linkage
∙ Community facility linkage

Internal facility linkage

Inter-facility linkage refers to connecting a newly diagnosed patient at one department to another department in the same facility for HIV treatment, care, and support services.

Steps of internal linkage facilitation

Post-test counseling

∙ Provide results accurately
∙ Provide information about care available at facility and elsewhere in catchment area ∙ Describe the next care and treatment steps
∙ Discuss the benefits of early treatment initiation and cons of delayed treatment ∙ Identify and address any barriers to linkage
∙ Involve the parent and child in the decision-making process regarding care and treatment ∙ Fill in client card and include referral notes
∙ Fill in the triplicate referral form
∙ Introduce and hand the patient to a linkage facilitator
∙ If same day linkage is not possible, book an appointment for the client at the clinic and follow-up to ensure the patient attends

Patient is escorted to the HIV clinic

∙ Linkage Facilitator escorts client to ART clinic with the linkage forms
∙ Hand over client to responsible staff at that clinic

Enrolling at HIV clinic

∙ Register the patient in the pre-ART register
∙ Open an HIV/ART card/ file for the patient
∙ Offer ART preparatory counseling
∙ Conduct baseline investigations
∙ If the patient is ready to start ART, initiate ART and continue with counseling support (disclosure, psychosocial)
∙ Coordinate integrated care if require (e.g. TB/HIV treatment,
∙ PMTCT)
∙ Discuss and make an appropriate appointment with the patient

Inter facility linkage

Inter-facility linkage refers to connecting a newly diagnosed patient at one facility to another facility for HIV treatment, care, and support services.

The referring facility should track (follow up) all HIV-positive patients referred to other facilities and ensure they are enrolled in care and on ART within 30 days, using the follow up/tracking schedule.

Community-facility-community linkages

Community-facility linkage refers to connecting a client who tests HIV-positive in the community to a health facility for HIV treatment, care, and support services.

HTS programs should establish functional community health systems with linkage systems including Peer Leaders, Expert Clients, VHTs and CHEWs. These should be involved in the mobilization for the targeted outreaches and follow up to link all who testing positive. Linkage from community to facility should be done within 30 days after diagnosis.

10 point care package for comprehensive Pediatrics AIDS care

1∙ Confirm HIV status as early as possible

2∙ Monitor the child’s growth and development

3∙ Ensure Immunizations are started & completed as per schedule

4∙ Provide prophylaxis for OI

5∙ Actively look for and treat infections early

6∙ Counsel mother & family on:

∙ Optimal infant feeding
∙ Good personal & food hygiene
∙ Follow up recommendations for the child

7∙ Conduct disease staging for the infected child

8∙ Offer ARV treatment for the infected child, if needed

9∙ Provide psychosocial support for the infected child and mother

10∙ Refer the infected child to higher levels of specialized care if necessary

Treatment of HIV/AIDS in Children (ARV therapy)

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Clinical Manifestation of HIV / AIDS in Children

On history taking

Unusually frequent and severe occurrences of common childhood bacterial infections, such as otitis media, sinusitis, and pneumonia
Recurrent fungal infections, such as candidiasis (thrush), that do not respond to standard antifungal agents: Suggests lymphocytic dysfunction
Recurrent or unusually severe viral infections, such as recurrent or disseminated herpes simplex or zoster infection or cytomegalovirus (CMV) retinitis; seen with moderate to severe cellular immune deficiency
Growth failure
Failure to thrive
Wasting
Failure to attain typical milestones: Suggests a developmental delay; such delays, particularly impairment in the development of expressive language, may indicate HIV encephalopathy ∙ Behavioral abnormalities (in older children), such as loss of concentration and memory, may also indicate HIV encephalopathy

During Physical examination inclusive of investigations

Candidiasis: Most common oral and mucocutaneous presentation of HIV infection ∙ Thrush in the oral cavity and posterior pharynx: Observed in approximately 30% of HIV-infected children
Linear gingival erythema and median rhomboid glossitis
Parotid enlargement and recurrent aphthous ulcers
Hepatic infection with herpes simplex virus (HSV): May manifest as herpes labialis, gingivostomatitis, esophagitis, or chronic erosive, vesicular, and vegetating skin lesions; the involved areas of the lips, mouth, tongue, and esophagus are ulcerated
HIV dermatitis: An erythematous, papular rash; observed in about 25% of children with HIV infection
Dermatophytosis: Manifesting as an aggressive tinea capitis, corporis, versicolor, or onychomycosis ∙ Pneumocystis jiroveci (formerly P carinii) pneumonia (PCP): Most commonly manifests as cough, dyspnea, tachypnea, and fever
Lipodystrophy: Presentations include peripheral lipoatrophy, truncal lip hypertrophy, and combined versions of these presentations; a more severe presentation occurs at puberty ∙ Digital clubbing: As a result of chronic lung disease
Pitting or non-pitting edema in the extremities
Generalized cervical, axillary, or inguinal lymphadenopathy

Signs/conditions very specific to HIV infection

Pneumocystis pneumonia
Esophageal candidiasis
Extrapulmonary cryptococcosis
Invasive salmonella infection
Lymphoid interstitial pneumonitis
Herpes zoster (shingles) with multi-dermatomal involvement
Kaposi’s sarcoma
Lymphoma
Progressive multifocal encephalopathy

Signs/conditions common in HIV-infected children and uncommon in uninfected children

Severe bacterial infections, particularly if recurrent
Persistent or recurrent oral thrush
Bilateral painless parotoid enlargement
Generalized persistent non-inguinal Lymphadenopathy
Hepatosplenomegally (in non-malaria endemic areas)
Persistent and recurrent fever
Neurologic dysfunction
Herpes zoster, single dermatome
Persistent generalized dermatitis (unresponsive to treatment)

Conditions common in HIV-infected children but also common in ill uninfected children

Chronic recurrent otitis with ear discharge
Persistent or recurrent diarrhoea
Severe pneumonia
Tuberculosis
Bronchiectasis
Failure to thrive

Opportunistic Infections in Children

Common clinical conditions associated with HIV

Babies are born with an immature and immunologically naïve immune system, predisposing them to an increased frequency of bacterial infections. The immunosuppressive effect of HIV are additive to those of immature immune system and place HIV-infected infants at high risk of invasive bacterial infections. Common childhood infections and conditions are more frequent in HIV-infected children and have a higher case fatality compared to uninfected children. These infections include:
Diarrhea
Acute suppurative otitis media
Sinusitis
Failure to thrive
Immunization and cotrimoxazole prophylaxis significantly decreases the frequency of invasive bacterial infections in HIV-infected children.

Common Opportunistic Infections

Cytomegalovirus: presents with encephalitis with retinitis or neuritis
Cryptococcus: presents with fever, headache, seizures, change in mental status; focal neurological signs are uncommon
Toxoplasmosis: most common manifestations are encephalitis, mental changes, fever, headache, and mental confusion
Herpes simplex virus: is associated with fever, altered state of consciousness, personality changes, convulsions
Kaposi’s sarcoma: this presents as early as the first month of life. It is associated with human herpes virus and usually presents as generalized Lymphadenopathy, black/purple mucocutaneous lesions (skin, eye, mouth)
Bacterial pneumonia: It is the leading cause of hospital admissions and death in HIV infected children. Streptococcus pneumoniae is the most common pathogen isolated. Other organisms include: H. influenzae, staphylococcus aureus, Klebsiella.
Pneumocystis pneumonia (PCP): PCV is caused by a fungus called Pneumocystis jiroveci(formally known as pneumocystis carnii). It is a major cause of severe pneumonia and death in HIV-infected infants.
Tuberculosis: Tuberculosis and HIV-co-infection; The HIV pandemic has led to the resurgence of tuberculosis in both adults and children. Children are at increased risk of developing primary progressive tuberculosis because of the associated severe immune suppression resulting from their young age and HIV. There is a high fatality rate for children who are co-infected with tuberculosis and HIV.
Lymphoid interstitial pneumonia (LIP): LIP is common in children (occurs in about 40% of children with perinatal HIV) and usually occurs in children more than 2 years of age.
Viral pneumonitis: It develops due to a number of viruses, including respiratory syncytial virus, para-influenza virus, influenza virus, adenovirus, varicella, measles and Cytomegalovirus (CMV).

Examples of Opportunistic infections

Bacterial OIs

∙ Pneumococcal pneumonia
∙ Pulmonary tuberculosis
∙ Salmonellosis
∙ Extra-pulmonary tuberculosis

Viral OIs

∙ Herpes zoster
∙ Recurrent/disseminated viral herpes simplex

Parasitic OIs

∙ Pneumocystis cariini pneumonia
∙ Toxoplasmosis

Fungal OIs

∙ Cryptosporidium
∙ Oro-pharyngeal candida
∙ Candida Esophagitis
∙ Histoplasmosis
∙ Coccidioidomycosis,
∙ Cryptococcal meningitis

Opportunistic cancers

∙ Invasive cervical cancer (caused by human papilloma virus)
∙ Kaposi sarcoma (caused by human herpes virus 8 HHV-8)
∙ Non Hodgkin lymphoma

Causes of opportunistic infections in HIV/AIDS children

∙ Poor adherence to treatment
∙ Presence of other diseases e.g. juvenile diabetes mellitus
∙ Delay in identification of the Infection
∙ High viral load
∙ Poor nutrition
∙ Exposure to opportunistic infectious agents
∙ Ingestion of substances contaminated with opportunistic infectious agents ∙ Missing out immunization programs
∙ Poor hygiene of the child
∙ Poor sanitation
∙ Poor ventilation

Prevention of opportunistic infections

∙ Avoidance of contact with the disease agents
∙ Proper treatment of other underlying diseases
∙ Adherence on HIV drug treatment
∙ Immunization of children against killer diseases
∙ Ensuring that children eat well cooked food and boiled water
∙ Early identification and treatment of the opportunistic diseases ∙
∙ Health education of the family and infected child about opportunistic infection

General management of opportunistic infections

Assessment of the child

⇒ History taking from the mother/caregiver and the child if he/she is verbal ∙ Physical examination

⇒ Vital observations

⇒ Head to toe examinations

⇒ Investigations e.g. blood microscopy e.t.c

Provision of treatment

No.	Type of infections	Drugs of choice
1.	Fungal infections	Anti – fungals
2.	Bacterial infections	Anti – bacterials
3.	Viral infections	Anti – virals
4.	Parasitic	Anti – protozoa
5.	Cancers	Cytotoxic drugs

WHO CLINICAL STAGING OF HIV

Staging HIV infection and disease in children

Staging is a standardized method for assessing disease stage/progression and for making treatment decision. Clinical and laboratory parameters are used to stage HIV disease.

WHO staging for HIV infection and disease in children above 10 years

Clinical Stage I:

Asymptomatic
Persistent generalized lymphadenopathy

Clinical Stage II:

Moderate weight loss (less than 10% of presumed or measured body weight)
Minor muco-cutaneous manifestations (seborrhoeic dermatitis, prurigo, fungal nail infections, recurrent oral ulcerations, angular stomatitis)
Herpes zoster within the last five years
Recurrent upper respiratory tract infections, e.g., bacterial sinusitis, tonsillitis, otitis media and pharyngitis

Clinical Stage III:

Severe weight loss (more than 10% of presumed or measured body weight)
Unexplained chronic diarrhea for more than one month
Unexplained prolonged fever, intermittent or constant, for more than one month 4. Oral candidiasis
Oral hairy leukoplakia
Pulmonary tuberculosis (current)
Severe bacterial infections such as pneumonia, pyomyositis, empyema, bacteremia or meningitis 8. Acute necrotizing ulcerative stomatitis, gingivitis or periodontitis.
Unexplained anemia (<8gm/dl), neutropenia (<0.5× 109 per liter), or chronic thrombocytopenia (<50× 109 per liter)

And/or Performance Scale 3: Bed-ridden for less than 50% of the day during the last month

Clinical Stage IV:

HIV wasting syndrome – weight loss of more than 10%, and either unexplained chronic diarrhea for more than one month or chronic weakness or unexplained prolonged fever for more than one month
Pneumocystis pneumonia (PCP)
Recurrent severe bacterial pneumonia
Toxoplasmosis of the brain
Cryptosporidiosis with diarrhea for more than one month
Chronic isosporiasis
Extra-pulmonary cryptococcosis including meningitis
Cytomegalovirus infection (retinitis or infection of other organs)
Herpes simplex virus (HSV) infection, mucocutaneous for more than one month, or visceral at any site
Progressive multifocal leukoencephalopathy (PML)
Any disseminated endemic mycosis such as histoplasmosis, coccidioidomycosis
Candidiasis of the oesophagus, trachea, bronchi or lungs
Atypical mycobacteriosis, disseminated
Recurrent non-typhoid salmonella septicemia
Extra-pulmonary tuberculosis
Lymphoma
Invasive cancer of the cervix
Kaposi’s sarcoma
HIV encephalopathy – disabling cognitive and/or motor dysfunction interfering with activities of daily living, progressing slowly over weeks or months, in the absence of concurrent illness or condition other than HIV infection that could account for the findings.
Atypical disseminated leishmaniasis
Symptomatic HIV-associated nephropathy or symptomatic HIV-associated cardiomyopathy And/or Performance Scale 4: Bed-ridden for more than 50% of the day during the last month

WHO staging for HIV infection and disease in infants and children

Clinical Stage I:

Asymptomatic
Persistent generalized lymphadenopathy

Clinical Stage II:

Unexplained persistent hepatosplenomegaly
Papular pruritic eruptions
Extensive wart virus infection
Extensive molluscum contagiosum
Recurrent oral ulcerations
Unexplained persistent parotid enlargement
Linear gingival erythema
Herpes zoster
Recurrent or chronic upper respiratory tract infections (otitis media, otorrhoea, sinusitis, tonsillitis)
Fungal nail infections

Clinical Stage III:

Unexplained moderate malnutrition not adequately responding to standard therapy
Unexplained persistent diarrhea (14 days or more)
Unexplained persistent fever (above 37.5 ºC, intermittent or constant, for longer than one month)
Persistent oral candidiasis (after first six weeks of life)
Oral hairy leukoplakia
Acute necrotizing ulcerative gingivitis/periodontitis
Lymph node Tuberculosis
Pulmonary Tuberculosis
Severe recurrent bacterial pneumonia
Symptomatic lymphoid interstitial pneumonitis
Chronic HIV-associated lung disease including bronchiectasis
Unexplained anaemia (<8.0 g/dl), neutropenia (<0.5 x 109/L3) or chronic thrombocytopenia (<50 x 109/ L3)

Clinical Stage IV:

Unexplained severe wasting, stunting or severe malnutrition not responding to standard therapy
Pneumocystis pneumonia (PCP)
Severe recurrent bacterial infections (e.g. empyema, pyomyositis, bone or joint infection, meningitis, but excluding pneumonia)
Chronic herpes simplex infection; (oro labial or cutaneous of more than one month’s duration, or visceral at any
site)
Extra-pulmonary Tuberculosis
Kaposi’s sarcoma
Oesophageal candidiasis (or Candida of trachea, bronchi or lungs)
Toxoplasmosis of the brain (after the neonatal period)
HIV encephalopathy
Cytomegalovirus (CMV) infection (retinitis or infection of other organs) with onset at age over one month
Extra-pulmonary cryptococcosis (including meningitis)
Disseminated endemic mycosis (extra-pulmonary histoplasmosis, coccidiomycosis)
Chronic cryptosporidiosis (with diarrhea )
Chronic isosporiasis
Disseminated non-tuberculous mycobacteria infection
Cerebral or B-cell non-Hodgkin lymphoma
Progressive multifocal leukoencephalopathy
HIV-associated cardiomyopathy or nephropathy

Diagnostic Measures

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Clinical Manifestation of HIV / AIDS in Children Read More »

HIV & AIDS in Children

HIV (Human Immunodeficiency Virus) is a unique type of virus (i.e. a retrovirus) that invades the T- helper cells (CD4 cells) in the body of the host (defense mechanism of a person).

AIDS (Acquired Immunodeficiency Syndrome) is a disease of the human immune system caused by infection with human immunodeficiency virus. In children it is acquired perinatally or by vertical -maternal-infant transmission.

HIV is the virus that causes AIDS

Introduction to HIV & AIDS in Children.

Considerable progress has been made towards eliminating human immunodeficiency virus (HIV) among children; however, the global burden of pediatric HIV and acquired immune deficiency syndrome (AIDS) remains a challenge for health care workers around the world, particularly in developing countries.

Epidemiology

Each day, some 1500 children under 15 years of age become infected with HIV, an estimated 90% of whom live in sub-Sahara-Africa. In 2005, there were 2.3 million (1.7–3.5 million) children living with HIV worldwide, most of whom acquired the virus in utero, during birth or while being breastfed, ways of contracting HIV that can be prevented.

For many children infected with HIV, the chances of survival are slim. Worldwide, AIDS now accounts for 3% of deaths in children under five years of age—and 6% of those in sub-Saharan Africa, where AIDS has become one of the major killers of young children.

One in seven people dying of HIV-related illness worldwide is a child under 15 years old. This is due largely to the failure to introduce programs for preventing mother-to-child transmission of HIV on the scale needed. Without HIV care, including antiretroviral therapy, the progression of HIV infection in children is particularly aggressive. In 2005, an estimated 380 000 (290 000–500 000) children died of HIV-related causes. It is likely that one half of them did not live past their second birthday.

Mode of Transmission

There are several potential modes of transmission of HIV to children:

Mother to child transmission: more than 95% of HIV-infected infants in Africa acquire HIV from their mothers during pregnancy, at the time of delivery, or potentially through breast feeding. Without any intervention, between 30 to 40% of breast-feeding HIV positive women transmit HIV to their newborns.
Sexual transmission among adolescents
Sexual abuse of children
Transfusion of infected blood or blood products
Unsterile injection procedures, and scarification

Risk factors for mother to child HIV-transmission

The risk factors associated with maternal to child transmission include the following:

Maternal factors

Women with high viral load are more likely to transmit HIV to their newborns
Women with severe immunosuppression (CD4 count below 200) and those with advanced disease.
Maternal micronutrient deficiencies increase the risk of MTCT of HIV significantly
Prolonged rupture of membranes, chorioamnionitis, and STIs
During breastfeeding, cracked nipples and breast abscesses
HIV-1 is more readily transmitted from an HIV-infected woman to her infant than is HIV-2.

Infant factors

Prematurity
Breastfeeding
Oral thrush and oral ulcers
Invasive fetal monitoring
Birth order (first twin) in twin pregnancy

Pathogenesis

The human body is made out of millions of different cells. Each body cell often makes new cell parts in order to stay alive and to reproduce.
Viruses hide their own material inside the cells of the body, and then, when the body cells try to make new parts, they accidentally make new viruses as well.
HIV mostly enters cells of the immune system.
Although HIV infects a variety of cells, its main target is the T4-lymphocyte (CD4): a kind of white blood cell that is responsible for warning the immune system that there are invaders (diseases) in the body.
Once HIV binds to a cell structure, it hides its material inside the cell. This turns the cell into a sort of HIV factory.
HIV enters the CD4 cell VIRAL GP120- (fusion and entry)
Now, HIV enters the centre of the cell. To do this, it needs to make some important changes in the way it looks so that it will not be ‘recognized’ by the cell. HIV has a special substance to make these changes in its structure.- (reverse transcription)
HIV is present in the centre of the cell, but in a different shape- (integration to genome).
The centre of the cell starts to make new parts of HIV instead of making new parts for the body’s defence. (transcription and translation).
Before leaving the cell, the new parts of HIV need to be put together, just like parts of a car need to be put together in the factory before they can leave the factory to be sold. HIV has a special substance that helps to put the different parts together to form a new HIV before it leaves the cell- budding
HIV attacks many CD4 cells. The infected CD4 cells will first produce many new copies of the virus, and then die. The new copies of HIV will then attack other CD4 cells, which will also produce new copies of HIV and then die. This goes on and on: more and more CD4 cells are destroyed, more and more new copies of HIV are made, and new CD4 cells get infected.

Steps / Phases in HIV entry

CD4 & chemokine receptors are needed for HIV entry therefore the following are the phases

Viral Entry: Binding of gp 120, CD4 and chemokine receptors results in changes in gp41 and fusion of the virion and cell surface membrane. Strands of viral RNA are released into the cell cytoplasm
Reverse Transcription: In nature DNA produces RNA, but retroviruses can convert single stranded RNA into double stranded DNA using an enzyme called reverse transcriptase
Integration: Viral DNA integrates into the host chromosome DNA to form a provirus
Transcription: back to RNA. In activated lymphocytes, transcription of viral DNA results in production of multiple copies of viral RNA. HIV RNA has 9 genes which code for the production of structural proteins like the viral envelope and core, in addition to reverse transcriptase, integrase,
and protease
Translation: RNA to protein
Viral protease; Viral protease cleaves [cuts] the polypeptide chain into enzyme components like integrase and reverse transcriptase which help produce new virions
Assembly and budding: Viral RNA and proteins are packaged and released from lymphocyte surface

How HIV attacks the body.

The CD4 (white blood cell), is a friend of the body. Problems like cough, diarrhoea try to attack the body, but the CD4 fights them to defend the body, its friend.
Now, HIV enters and starts to attack the CD4. The CD4 notices it cannot defend itself against HIV. Soon, CD4 loses its fight against HIV. The body remains without defence.

The body is all alone, without defence, so all kinds of problems, like cough and diarrhoea take advantage and start to attack the body. In the end, the body is so weak that all diseases can attack without difficulty.

Clinical Manifestation of HIV / AIDS in Children

HIV & AIDS in Children Read More »

Bipolar Affective Disorder

Bipolar Affective Disorder is formerly called manic-depressive illness (MDI). B.A.D is severe and persistent condition that causes serious lifelong struggle and challenge.

Bipolar affective disorder is a mental health condition characterized by mood swings, from deep and prolonged low mood (profound depression) to extreme euphoria (mania), with intervening normal periods.

Episodes of mood swings may occur rarely or multiple times a year. While some people will experience some emotional symptoms between episodes, some may not experience any.

They are of three kinds i.e.

Mixed bipolar disorder that is both manic and depressive episodes intermixed
Manic bipolar disorder; here there is predominant elation of mood, irritability, excessive motor activity and evident psychotic features
Depressed bipolar disorder; symptoms are characteristic of major depression with a history of at least one manic episode.

Symptoms of bipolar affective disorder

Symptoms of bipolar vary from person to person and from time to time depending on the phase the patient is in.

Manic episode

Manic episodes have at least 1 week of profound mood disturbance characterized by elation and irritability at least 3 of the following;

grandiosity
Increased energy, activity (boundless energy)
Exaggerated sense of well-being and self-confidence (euphoria)
Decreased need for sleep
Unusual talkativeness
Racing thoughts or flight of ideas
Distractibility
Poor decision making for example taking sexual risks or making foolish investments

Hypomanic episode

This is characterized by elated or irritable mood of at least 4 consecutive days duration. The diagnosis of hypomania requires at least 3 of the above symptoms the difference being that here the symptoms are not severe enough to cause marked impairment in social or occupational functioning

Depressive episode

In a major depressive episode, for the same 2 weeks a person may experience 5 or more of these symptoms with at least one of the symptoms being either depressed mood or loss of pleasure or interest.

Depressed mood, such as feeling sad, hopeless, tearfulness and irritability in children and teens
Marked loss of interest or feeling of no pleasure in almost all activities
Significant weight loss when not dieting
Psychomotor retardation or agitation
Either insomnia or sleeping too much (hypersomnia)
Either restlessness or slowed behaviour
Fatigue or loss of energy
Feelings of worthlessness or excessive or inappropriate guilt
Decreased activity to think or concentrate
Thinking about, planning or attempting suicide
Melancholia; this refers to depression not triggered by a stressor

Management of bipolar affective disorder

The treatment of bipolar affective disorder is directly related to the phase of episode (i.e. depression or mania and the severity of that phase.

MANIA

Mania is condition characterized by excessive or extreme elation of mood and increased activity.

It is a state of mind manifesting with cheerfulness, euphoria, and rapidly changes to irritability.

Types of mania

Hypomania: This is a mild form of mania

Acute mania: Acute, severe and heavy form of mania

Delirious mania: Excitation characterized by confusion mainly found in organic psychoses.

Chronic mania: Mania that has occurred in the patient, it could be simple form but has failed to respond to various forms of treatment. It usually occurs in people 40 years and above.

CAUSES OF MANIA

Genetic factors; mania is said to run in families
Increase in levels of noradrenaline metabolites
Imbalances in serotonin levels in blood
Increase in dopamine levels
Cyclothymic type of personality (mood swings) plays a big role in the causation of manic illness occurrence.
Body physic;
Psychosocial factors like those resulting from stresses e.g. Divorce, bereavement etc.

Clinical features of mania

Elation of mood
Great deals of energy (boundless energy)
Usually restless and over active
Poor concentration and easily destructed by other activities
Patients have high appetite for food and drinks but usually have no time to eat since they lack concentration
Increased urge for sex (high libido)
Excessive involvement in pleasurable activities e.g. excessive spending habits
Dressing is usually inappropriate with bright colours that do not match, excessive make-up and jewelery.
Delusions of grandeur are more pronounced
Over talkativeness and pressure of speech in acute forms of mania
Racing thoughts i.e. accelerated thinking (the speech is very fast and continuous)
Insight is lost
Sleep is disturbed and a patient may have total insomnia
Auditory hallucinations are very common
Ideas of reference are very common (when the patient feels that people are conversing about him)

Diagnosis of mania

The following features are diagnostic of mania;

Abnormally elevated mood and irritability
Grandiosity (over rating one’s self)
Boundless energy
Over activity
Over talkativeness
Racing of thoughts
Poor concentration and easily destructed.

Management

Hypomanic can be managed at home if there is someone to assist them take their medications

Hospitalization: If the patient is too excited, is a public nonsense, not taking care of himself e.t.c. then admission to mental health hospital is very essential.

Establishment of therapeutic relationship is very important because, it`s the key to the nursing care.
If the patient is very excited, restless and unable to be calm down by the verbal instruction of the care team, a tranquilizer or a sedative such as chlorpromazine 100-200mg or Haldol 5-10mg by injection are administered
Reduce the dosage and frequency as the symptom subsides.
Short simple direct answers should be given when a patient asks questions.
Ensure a low stimuli of the patient`s environment.
Remove all the dangerous particles like iron bars, sharp instruments, easily portable stone etc that the patient can use to harm himself and others.
Supervise and maintain personal hygiene.
Special attention must be given to patient’s diet because a patient is usually too busy to eat because of hyperactivity and restlessness. diet rich in carbohydrates, proteins with a lot of fluids is recommended.
Observe the patient behaviors, toilet habits, eating habits, steep etc

DRUG TREATMENT

To control the manic symptoms antipsychotic like Haldol or chlorpromazine can be used.

CPZ (chlorpromazine) 100-1200mg in divided doses which may be reduced when the patient improves

Thioridazine 100-600mg in divide doses (it can also help to lower the patient libido)
Haloperidol: 5-15mg nocte for not more than to work
Lithium carbonates: 250-550mg doses (it is the drug of of choice in manic patients)
Benzelhexol (artane)

Other drug used in manic illness in

Carbamazepine: 100-400mg in divided doses
Sodium volporate: 100-1500mg in divided doses (but are usually given given in carbonates).

ELECTRO COMVULSIVE THERAPY

This is very good especially in manic excitement. 1 or 2 shocks a week for 6-9 weeks. ECT is very effective when given in combination with drugs.

OCCUPATIONAL THERAPY

Occupational therapy is very important for recovering patient and the type of occupation varies from individual patient to another.
Psychotherapy to the family is very helpful
Resettlement and good follow up system should be put in place for individual patient.

Nursing care of manic patients

Diet; special attention has to be given to patients diet because he is usually too busy to eat and hence may lose weight and also dehydration may occur.
Meals and fluids have to be given under supervision and extra nourishment may be required to compensate for extra activity.
Care has to be taken to ensure that the patient dresses well
Supervision and directions to maintain personal hygiene like bathing, oral hygiene is essential.
one nurse has to be assigned to the over active patient so as to improve his confidence in her
Maintain a low level of stimuli to the patient environment i.e. Factors like noise and bright colours should be avoided in the ward otherwise the ward should be quiet and pleasant.
observe patients behaviour frequently and report any changes
remove any dangerous objects from the patients environment that can be used to harm self or others during times of agitation
Injuries attained by the patient because of his hyperactivity have to be attended to.

Prognosis

If well treated, most episodes resolve within three months and rarely last for more than 6months
There is risk of reoccurrence if the disorder begins before 30years of age
Studies have revealed that 10-20% of the sufferers have had 3 episodes of depression before developing mania
The prognosis of mania is far better than that of schizophrenia

Bipolar Affective Disorder Read More »

Mood Disorders in Children and Adolescents

Mood Disorders In Children and Adolescents

Mood disorders are chronic, often debilitating illnesses that affect people of all ages.

Mental health problems ranging from depression to bipolar disorder are known as mood disorders, or affective disorders. In any of these disorders, a serious change in mood shapes the child’s emotional state. Unlike a normal bad mood a child feels occasionally, a mood disorder involves thoughts and feelings that are intense, difficult to manage, and persistent. A mood disorder is a real medical condition, not something a child will likely just “get over” on his own.

Today, clinicians and researchers believe that mood disorders in children remain one of the most under diagnosed health problems. Mood disorders that go undiagnosed can put children at risk for other conditions, like disruptive behavior and substance use disorders, that remain after the mood disorder is treated. Children and teens with a mood disorder don’t always show the same symptoms as adults. So it can be difficult for parents to recognize a problem in their child, especially since he or she may not easily express his or her thoughts or feelings.

The most common mood disorders in children and adolescents include:

Major depression. A depressed or irritable mood, lasting at least two weeks.
Persistent depressive disorder (dysthymia). A chronic, low-grade, depressed or irritable mood for at least 1 year.
Bipolar disorder. Periods of persistently elevated mood followed by periods of depressed or flat emotional response.
Disruptive mood dysregulation disorder. A persistent irritability and extreme inability to control behavior.
Premenstrual dysphoric disorder. This includes depressive symptoms, irritability, and tension before menstruation.
Mood disorder due to a general medical condition. Many medical illnesses, including cancer, injuries, and chronic medical illnesses, can trigger symptoms of depression.
Substance-induced mood disorder. Symptoms of depression due to drug use, the effects of a medication, or exposure to toxins.

Girls are at least twice as likely as boys to develop depression. Boys and girls are equally likely to develop bipolar disorder and obsessive-compulsive disorder.

Causes

The causes of mood disorders are not well understood. however the following can be attributed to;

Imbalances in brain chemicals.
Environmental factors, such as unexpected life events and/or chronic stress, can also contribute to a mood disorder.
Mood disorders often run in families, so there is a genetic component, too. Children who have relatives with depression are at increased risk for depression. In addition, a family history of bipolar disorder may predispose a child to have bipolar disorder or other mood disorder.
Sometimes, extreme stress or a life event can “turn on” a gene, causing the disorder to develop. This can happen especially with depression.

Signs and Symptoms

Children show symptoms differently, according to their age and biological makeup. Symptoms also vary according to the type of mood disorder. Overall signs of a mood disorder may include:

Sad, depressed, irritable, angry, or elevated mood that appears more intense than the child usually feels, lasts for a longer period of time, or occurs more frequently
Trouble with family, including difficult behavior
Lack of motivation or pleasure in previously enjoyed activities
Changes in sleep or eating patterns or weight
Frequent physical complaints, such as headaches, stomachaches, or fatigue
Loss of energy or fatigue
Difficulty achieving in school
Worthlessness, guilt, or low self-esteem
Severe recurrent temper outbursts
Increased energy or bursts of energy with racing thoughts or fast speech
Rebellious or high risk behavior
Running away or threats of running away from home
Difficulty with friends and peers
Expressions of suicidal thoughts, which should be evaluated immediately

Diagnosis

An accurate diagnosis of the mood disorder, as well as any other conditions, is a crucial first step in managing the disorder effectively. At the Hospital, a specialist performs a comprehensive evaluation. The evaluation may assess:

child’s overall health and medical history
child’s symptoms
child’s behavior at home, at school, and with peers
Environmental factors that might be stressors in your child’s life
Input from teachers or guidance counselor about issues at school
child’s past experiences with specific medications or therapies
opinion or preference for treatment options

Treatment

Mood disorders can be treated with evidence-based treatments, especially with early recognition of the problem. Treatment can help manage the episode, reduce the severity of symptoms, and help to prevent future episodes. It can also enhance the child’s normal growth and development and improve his or her quality of life and relationships.

Individual therapy

identify key problems in the child’s life and help the child learn how to manage these stressors.
Also use a variety of techniques to help the child manage the symptoms of the mood disorder, including
- Cognitive-behavior. This approach involves changing problematic thoughts, feelings, and behaviors that your child may be experiencing.
- Interpersonal therapy. This technique focuses on building social skills and helping children with difficult relationships in their lives.
Family therapy

Families play a vital supportive role in any mood disorder. Families, including parents or guardians, can learn methods to help their child manage mood and behavior problems. The specialist may also explore potential stressors in a child’s life and patterns of interaction within the family. A consultation with the child’s teachers or guidance counselor may also be advised.

Medications

A variety of medications are very effective in treating mood disorders by altering the brain chemicals involved. Depending on the mood disorder and the child’s symptoms, medications may reduce the severity or frequency of symptoms, decrease problematic behaviors, improve functioning, and prevent future episodes.

Outlook

Many children who receive early and adequate treatment for their mood disorder may improve significantly and keep their condition managed with ongoing intervention or support . If the episodes recur, they can usually be managed with therapeutic support, including medications, therapy, and additional resources.

Follow-up Care

Depending on the child’s personalized treatment plan, the child and family may continue to meet with the specialist for a number of weeks or months. The focus of individual and family therapy may change over time, depending on the child’s age, progress, and needs. Medication needs may also change over time depending on a number of factors.

SPECIFIC MANAGEMENT OF MOOD DISORDERS.

Assessment 🕵️‍♀️
- Conduct thorough assessments to understand the child’s mood disorder, including emotional triggers and symptoms.
Supportive Environment 🌈
- Create a safe and nurturing environment to promote emotional well-being.
Therapeutic Communication 🗣️
- Utilize effective communication techniques to build trust and encourage expression of feelings.
Medication Management 💊
- Administer prescribed medications as directed, and monitor for any side effects or changes in mood.
Psychotherapy 🧘‍♀️
- Encourage participation in individual or group therapy sessions to address underlying issues.
Education 📚
- Provide education to both the child and their family about the mood disorder, coping strategies, and treatment options.
Behavioral Interventions 🧩
- Implement behavior modification techniques to manage disruptive behaviors and promote positive coping mechanisms.
Emotion Regulation 🧘‍♂️
- Teach the child emotional regulation skills, such as mindfulness and relaxation techniques.
Family Involvement 👪
- Engage the family in therapy and support, as their understanding and involvement are crucial.
Safety Monitoring 🚸
- Continuously monitor the child’s safety to prevent self-harm or harm to others, especially in severe cases.

BIPOLAR AFFECTIVE DISORDER click here

Mood Disorders in Children and Adolescents Read More »

Osteomyelitis

Cause

Wald Vogel Classification of Osteomyelitis

Pathophysiology of Osteomyelitis

PREDISPOSING FACTORS

Signs and Symptoms of Osteomyelitis.

Management of Osteomyelitis

Nursing Care

Nursing Diagnosis

Ineffective Tissue Perfusion Interventions:

Hyperthermia Interventions:

Acute Pain Intervention

Complications

Osteopenia of Prematurity

Causes

Signs and symptom

Pathophysiology

Risk Factors

Diagnosis and Investigations

Management

Fractures

Causes of Fractures

Classification of Fractures

Signs and symptoms of fractures

Assessment and Diagnostic Findings

Process of Fracture Healing

Healing of Fractures

Management

First aid management

COMPLICATIONS OF FRACTURES

Related Question

Prevention and Control of HIV/AIDS

Prevention in Pediatrics

BEHAVIORAL CHANGE AND RISK REDUCTION INTERVENTIONS

Biomedical prevention interventions

Post-exposure prophylaxis (PEP)

ORAL PRE-EXPOSURE PROPHYLAXIS (PrEP)

MOTHER-TO-CHILD TRANSMISSION OF HIV

Treatment Modalities of HIV/AIDS

ANTIRETROVIRAL DRUG TREATMENT

Principles for selecting the ARV regimens

Available ARVs in Uganda

Uses of ART (Antiretroviral Therapy)

Recommended First Line Regimens in Adults, Adolescents, Pregnant Women and Children

RECOMMENDED FIRST-LINE REGIMEN FOR INITIATION OF ART IN CHILDREN UNDER 3 YEARS OF AGE

WHAT REGIMEN TO SWITCH TO (SECOND-LINE AND THIRD-LINE ART)

Monitoring of ARV Treatment

Methods of Monitoring ARV Treatment

Viral Load Monitoring

CD4 Monitoring

Other Laboratory Tests

Problems Associated with ARV Treatment

Immune Reconstitution Inflammatory Syndrome (IRIS)

Steps to Reduce IRIS Development

ARV Drug Toxicity

Management of ARV Side Effects/Toxicities

Dosages of Nevirapine

Counselling on Infant Feeding Choice

Feeding Options

If Mother Chooses Breastfeeding

If Mother Chooses Replacement Feeding

Treatment of HIV/AIDS in Children (ARV therapy)

Diagnostic Measures / Investigations.

HIV testing provision steps/protocol

Principles of HIV testing services (HTS)

Places to prick a child

HIV testing algorithm for infants and children below 18 months of age

Procedure for DBS collection

Cautions during HIV testing

LINKAGE FROM HIV TESTING TO HIV PREVENTION, CARE AND TREATMENT

Types of linkages

Internal facility linkage

Inter facility linkage

Community-facility-community linkages

10 point care package for comprehensive Pediatrics AIDS care

Clinical Manifestation of HIV / AIDS in Children

Opportunistic Infections in Children

Common Opportunistic Infections

Examples of Opportunistic infections