​Kembara Xtra - Medicine- Cerebral Palsy 
Introduction 

A collection of clinical conditions known as cerebral palsy (CP) are defined by motor and postural dysfunction as a result of long-lasting, nonprogressive abnormalities in the developing brain. A motor disability that limits activity is required for this diagnosis. The type of mobility dysfunction and the functional severity of CP are used to categorize it.

Epidemiology (Incidence and Prevalence) Incidence: 1.5 to 3.0 per 1,000 live births overall; incidence rises as gestational age (GA) at birth falls:
The incidence rises as birth weight decreases: - 146/1,000 for GA of 22 to 27 weeks; - 62/1,000 for GA of 28 to 31 weeks; - 7/1,000 for GA of 32 to 36 weeks; - 1/1,000 for GA of 37+ weeks.


Pathophysiology and Etiology 

 Multifactorial; CP is caused by lesions or static injuries to the developing brain that can happen before birth, during pregnancy, or after birth.
Free radicals, cytokines, and the inflammatory response are probably contributing elements.
The most frequent kind of cerebral palsy (CP) is spastic, and it usually results from either periventricular leukomalacia or germinal matrix hemorrhage.
Genetics There have been studies linking CP to polymorphisms in the thrombophilic, cytokine, and apolipoprotein E genes.

Risk factors include breech birth, preterm delivery, low birth weight, periventricular leukomalacia, perinatal hypoxia/asphyxia, intrauterine growth retardation (IUGR), multiple gestations, in utero stroke, clinical and histologic chorioamnionitis, antepartum bleeding, maternal factors (cognitive impairment, seizure disorders, hyperthyroidism), and abnormal fetal position (e.g., breech
Postnatal: increasing hydrocephalus, sepsis, meningitis, encephalitis, traumatic brain injury or stroke,

Prevention
Effective preventive measures include magnesium sulfate, newborn hypothermia, and prenatal corticosteroids.
Using magnesium sulfate to treat women during preterm delivery is neuroprotective for the fetus and may lower the chance of CP. Unknown is the effect on a term fetus.

 Therapeutic hypothermia is beneficial for term babies who endure intrapartum hypoxia.

Accompanying Conditions 

Seizure disorder, behavioral issues, hearing and vision difficulties, and intellectual and speech and language disabilities.

Decreased linear growth and weight abnormalities (underweight and overweight) Osteopenia Bowel and bladder incontinence Orthopedic: contractures, hip subluxation/dislocation, scoliosis (60%) GI conditions: constipation (59%), vomiting (22%), gastroesophageal reflux Poor dentition, excessive drooling GI conditions: gastroesophageal reflux

Guidelines for an early and precise diagnosis are as follows:
- International recommendations for CP early diagnosis before the age of 12 months: Neuroimaging, the Prechtl General Movements Assessment (GMA) before five months, and the longitudinal use of the Hammersmith Infant Neurologic Examination (HINE) (7) between three and twelve months are all tools for detection.


A clinical diagnosis that takes into account the following factors: - Delayed motor milestones; - Abnormal tone; - Abnormal neurologic exam suggesting a cerebral etiology for motor dysfunction; - Absence of regression (not losing function); - Absence of underlying disorders or other explanation for etiology
Although the pathologic lesion is unchanging, the infant's growth and development may cause changes in the clinical appearance.

Introducing History 

Discover the risk factors that are prenatal, perinatal, and postnatal.
the timing of motor milestones; poor nutrition; frequent vomiting; agitation; abnormal spontaneous general movements; and neurobehavioral symptoms.

 Asymmetries in movement, such as an early predilection for the hand
CP does not cause motor abilities to regress.


clinical assessment 
Spasticity causes increased tone, reflexes, and clonus; Dyskinesia causes abnormal movements; Hypotonia causes decreased tone; Ataxia causes abnormal balance and coordination; Tone can be increased or decreased; Trunk and head control are frequently poor but can be advanced due to high tone; Reduced strength and motor control; Persistence of primitive reflexes; Asymmetry of movement or reflexes; Decreased joint range of motion and contractures; Brisk deep tendon reflexes; Clon CP is categorized as follows:
- Spasticity Unilateral: hemiplegic Bilateral: quadriplegic (UE LE involvement) or diplegic (lower extremity [LE] > upper extremity [UE] involvement)
- Dystonia: increased rigidity and decreased mobility
Ataxia is a loss of ordered muscular coordination. Choreoathetosis is an irregular spasmodic involuntary movement of the limbs or face muscles. UE and fine motor skills can be evaluated using the Manual Ability Classification System (MACS).

Multiple Diagnoses 
Muscular dystrophy, benign congenital hypotonia, brachial plexus injury, familial spastic paraplegia, dopa-responsive dystonia, transient toewalking, metabolic illnesses (like glutaric aciduria type 1), mitochondrial disorders, and genetic abnormalities (like Rett syndrome) are just a few examples of conditions that could be present.

Diagnostic tests and laboratory results 
Although laboratory testing is not necessary to make a diagnosis, it might aid in ruling out alternative causes.
Testing for metabolic and genetic abnormalities should be taken into consideration if neuroimaging cannot identify a specific etiology or if the clinical presentation has unusual characteristics. In order to detect syndromes, certain brain abnormalities may require genetic or metabolic testing.
Children with cerebral infarction detected on neuroimaging due to hemiplegic CP should be given consideration for diagnostic testing for coagulopathies.

Initial examinations (lab, imaging)
Neuroimaging is not necessary, however it is advised for kids with CP whose etiology has not been determined.

CT should be replaced with MRI.

 80–90% of patients have one or more of the following abnormalities: periventricular leukomalacia, ventricular enlargement, intraventricular or other intracranial bleeding, brain malformation, cerebral infarction, or other abnormalities of the CSF space.

Diagnostic Techniques/Other Screening for comorbid conditions, such as feeding/swallowing issues, seizures, vision/hearing issues, speech and language abnormalities, and developmental delay/intellectual impairment.
Only if there is a history of possible seizures should electroencephalograms (EEGs) be taken.

Treatment 
Treatments that reduce spasticity to prevent painful contractures, manage comorbid disorders, and improve functionality and quality of life are centered on symptom control.

Early intervention for children ages 0 to 3 is a general treatment.
Several treatments improve function:
- Physical therapy to strengthen the muscles of the body, regulate movement, and avoid contractures.
- Occupational therapy to improve daily life activities that are functional
- Speech therapy to improve nutrition and verbal and nonverbal communication. - Equipment that maximizes activity participation:
Spinal bracing (body jacket) and orthotic splinting (ankle-foot orthosis) may delay the progression of scoliosis.
- Augmentative communication for nonverbal people using images, switches, or computers
- Wheelchairs, crutches, walkers, gait trainers, and standers for weight bearing


First Line of Medicine

Diazepam, a GABAA agonist that enables CNS inhibition at the spinal and supraspinal levels to diminish spasticity, is used as a temporary remedy for generalized spasticity; however, there is inadequate data on its effects on motor function.
– Negative consequences include ataxia and sleepiness
Pediatric dosage (children under 12 years old and under 15 kg): 0.5 to 1.0 mg HS; 8.5 to 15.0 kg: 1 to 2 mg HS; youngsters between the ages of 5 and 16 and under 15 kg: 1.25 mg TID
Botulinum toxin type A is injected directly into targeted muscles to treat localized spasticity; there is insufficient data on how it affects motor function. It has a higher functional benefit when combined with occupational therapy, and it lasts for 12 to 16 weeks after injection.

Next Line
A GABAB agonist called baclofen makes it easier for mono- and polysynaptic reflexes to be presynaptically inhibited.
Sedation and sleepiness are side effects.
- Symptoms of abrupt withdrawal include hyperthermia, hallucinations, convulsions, spasticity, and seizures.
Adults: Start with a dose of 5 mg TID and raise it every 3 days to a maintenance dose of 20 mg TID on average, with a daily maximum of 80 mg.
- Initial dose for children (>2 years): 10 to 15 mg/day. Increase to the highest effective dose of 40 milligrams per day. 60 mg/day maximum for children under 8; 60 mg/day maximum for children over 8
The continuous intrathecal method of baclofen (the baclofen pump) allows for a higher maximal response with a lesser dosage to alleviate spasticity.
- Adverse consequences include infection, catheter dysfunction, and CSF leakage - May improve gait in ambulatory adults but does not appear to benefit nonambulatory patients

Furthermore Treated 
Ophthalmology, neurology, orthopedics, physiatry, and physical, occupational, and speech therapists are all included in the multidisciplinary care.

Surgical Techniques 

 Dorsal root rhizotomy preferentially removes L1–S2 dorsal rootlets. Lower limb spasticity is reduced when combined with PT, although there are side effects. Regarding long-term results, there is insufficient evidence.
Surgery for gastrostomy, tendon lengthening, scoliosis management, joint subluxation, and dislocations

Suppportive Therapy 

Aquatherapy enhances gross motor function in patients with a range of motor severities, while therapeutic horseback riding and hippotherapy help patients with balance and postural control.
PERIODICAL CARE PROGNOSIS
Reduced lifespan is closely related to the severity of intellectual disability and functional impairment.

​​​Kembara Xtra - Medicine- Periorbital Cellulitis 
An acute bacterial infection of the skin and subcutaneous tissue that is located anterior to the orbital septum and does not affect the orbital structures (globe, fat, and ocular muscles).


Caution 
It is crucial to differentiate between orbital cellulitis and periorbital cellulitis. A potentially fatal condition is orbital cellulitis. The posterior to the orbital septum, orbital cellulitis manifests as proptosis, restricted eye movement, pain with eye movement, and altered vision.

(Incidence and Prevalence) Epidemiology 
3 times more prevalent than orbital cellulitis; more frequently occurs in children, mean age 21 months.

Incidence
Wintertime incidence is higher (as a result of an increase in sinusitis cases) 

Pathophysiology and Etiology 

The anatomy of the eyelid separates orbital cellulitis from periorbital (preseptal) cellulitis: - The orbital septum, a layer of connective tissue that runs from the orbital bones to the edges of the upper and lower eyelids, serves as a defense against infection of the deeper orbital structures.
- Periorbital (preseptal) cellulitis is an infection of the tissues located anterior to the orbital septum.
Periorbital cellulitis often results from a concurrent infection of soft tissues of the face, while orbital (postseptal) cellulitis is an infection that extends deep to the orbital septum.
- Extension of sinusitis (through lamina papyracea)
- Localized injuries; animal or insect bites - Foreign bodies
- Extensive dental abscesses
Hematopoietic seeding
Staphylococcus aureus is a typical common organism (MRSA is on the rise). - Streptococcus pyogenes - Staphylococcus epidermidis
Since the introduction of the vaccine, the incidence of Haemophilus influenzae disease has decreased (should still be suspected in unimmunized or partially immunized patients). Atypical organisms include Acinetobacter sp., Nocardia brasiliensis, Bacillus anthracis, Pseudomonas aeruginosa, Pasteurella multocida, Mycobacterium tuberculosis, and Trichophyton sp.
Genetics
No inherited tendency is known


Acute sinusitis, conjunctivitis, blepharitis, dental infection, localized skin damage or puncture wounds, insect bites, and bacteremia are risk factors.


Prevention
Avoid injuries near the eyes, swim with abrasions on your face in fresh or salt water, and get routine vaccinations, especially for H. influenzae type B and Streptococcus pneumoniae. 

Presenting History Periorbital soft tissue indulation, erythema, warmth, and/or discomfort, typically accompanied by normal vision and eye movements 
Chemosis (conjunctival edema), proptosis, and pain with extraocular eye movements are signs of orbital cellulitis and should be taken seriously in severe cases of periorbital cellulitis.

Alert
Fever, conjunctival edema, and pain with eye movement all point to orbital cellulitis.

clinical assessment 

Vital signs and appearance in general (Patients with ocular cellulitis frequently present with systemic illness.) 
Examine the skin, conjunctiva, lashes, and structures around the eyes.
Erythema, swelling, and discomfort of the eyelids without congested orbits - Violaceous eyelid coloring is more frequently linked to H. influenzae.
Check for skin deterioration.
In order to rule out herpetic infection, look for vesicles.
Check the sinuses and the nasal vaults for symptoms of acute sinusitis.
Test ocular motility and visual acuity. Inspect the mouth cavity for dental abscesses.

Differential diagnosis: Orbital cellulitis. Orbital cellulitis may present with similar symptoms to periorbital cellulitis, including fever, proptosis, chemosis, ophthalmoplegia, impaired visual acuity, and pain with ocular movement.
Rapidly progressing malignancies, such as Rhabdomyosarcoma, Retinoblastoma, Lymphoma, and Leukemia, as well as allergic inflammation, orbital or periorbital trauma, dacryocystitis, hordeolum (stye), and orbital myositis

Diagnostic tests and laboratory results 

Initial examinations (lab, imaging)
With differential, CBC
Blood cultures (poor yield), purulent discharge from wounds (if present), and blood cultures 
If there is a suspicion of orbital cellulitis (marked eyelid swelling, fever, leukocytosis, or failure to improve after taking the recommended antibiotics within 24 to 48 hours), imaging is advised.
CT to assess the level of infection and look for abscess or inflammation in the orbit: narrow (2 mm) sections of CT with contrast; coronal and axial images with bone windows – Bulging of the medial rectus on a CT scan is the typical indication of orbital cellulitis.


Tests in the Future & Special Considerations

Children with orbital or periorbital cellulitis frequently have sinusitis as an underlying condition.
Admission for blood cultures, antibiotic medication, and consideration of lumbar puncture should be made if a kid is febrile, under 15 months old, and appears toxic.

Administration of Medicine 
Use oral antibiotics to treat periorbital cellulitis and make sure you get close monitoring.
The most likely pathogens (Staphylococcus and Streptococcus) should be treated with empiric antibiotics.
Observe the prevalence of MRSA in your area to decide whether you need coverage.
In the case of simple periorbital cellulitis, there is no proof that IV antibiotics are superior to PO antibiotics in speeding up recovery or preventing secondary problems.
Uncomplicated posttraumatic periorbital cellulitis: This condition is typically brought on by skin bacteria, particularly Staphylococcus and Streptococcus. - Clindamycin 300 mg PO TID, doxycycline 100 mg PO BID, or trimethoprim-sulfamethoxazole (TMP-SMX) - Cephalexin 500 mg PO q6h or dicloxacillin 500 mg PO q6h If MRSA is suspected, give 1 to 2 DS tablets orally every 12 hours. 
Dental abscesses can be treated with amoxicillin-clavulanate 875 mg PO BID or clindamycin 300 mg PO TID. Bacteremic cellulitis, which may be linked to meningitis, can be treated with ceftriaxone 1 g IV q24h plus vancomycin 15 mg/kg/dose IV q8-12h or clindamycin 600 to 900 mg IV q8h to treat MRSA. - Therapy sessions should last 10 to 14 days on average. Follow patients closely (daily follow-up until improvement occurs) when they are given oral antibiotics for suspected periorbital cellulitis to monitor antibiotic response and potential progression to orbital cellulitis. The need for IV antibiotic therapy should be reevaluated if symptoms do not subside within 24 hours.

Questions that need more consultation

If there is worry for orbital cellulitis or if individuals don't improve promptly after receiving first-line treatment, consult ENT and ophthalmology.

Surgery is typically not recommended in straightforward circumstances. Orbital surgery is recommended if there is an abscess or a probable impairment of vital structures. The strongest clinical indicator of need for surgery is diplopia.

Admission Requirement 
Mild cases in adults and children over the age of one year old can be safely addressed on an outpatient basis if the patient is stable and there are no systemic signs of toxicity.
Think about receiving IV antibiotics and hospitalization: - If the patient displays systemic illness
- Infants and toddlers (3),(4)[C]
If patients do not improve or deteriorate within 24 hours of oral antibiotics, they may not have received S. pneumoniae or H. influenzae vaccinations. No set rules specify when to transfer from parenteral to PO medication. - High suspicion for orbital cellulitis (eyelid edema with decreased vision, diplopia, aberrant light responses, or proptosis). Once eyelid edema and erythema have greatly diminished, switching from IV to PO antibiotics is generally acceptable.
An antibiotic regimen of 10 to 14 days is recommended.


patient observation

Keep an eye out for symptoms of orbital involvement, such as impaired vision or painful or restricted ocular movement.

Patient Education Observe proper skin care.
Avoid skin trauma, and if it returns after receiving treatment, report any early skin changes (swelling, redness, and pain).

Prognosis: Patients have good outcomes when given prompt care.
Recurrent periorbital cellulitis must be distinguished from treatment failure brought on by antibiotic resistance when it involves three or more periorbital infections in a 12-month period.


Complications include scarring, loss of vision, cavernous sinus thrombosis, orbital abscess formation, and osteomyelitis.

​Kembara Xtra - Medicine- Orbital Cellulitis  
Postseptal cellulitis is the name for an acute, severe infection of the orbital contents that threatens eyesight and is located posterior to the orbital septum. Preseptal cellulitis, also known as periorbital cellulitis, is located anterior to the septum. The best workup and treatment are based on location.
Alternative name(s): postseptal cellulitis

Epidemiology (Incidence and Prevalence) Orbital cellulitis is substantially less prevalent than preseptal cellulitis; there is no difference in frequency between genders in adults; boys have a higher incidence in childhood.
Incidence
Since the advent of routine Haemophilus influenzae type b (Hib) immunization, the incidence of orbital cellulitis has decreased.


Pathophysiology and Etiology 

Sinusitis and orbital cellulitis are frequently linked.
Preseptal cellulitis is frequently accompanied by local skin problems on the eyelids and eyelashes.
The lamina papyracea ("layer of paper"), a small bony barrier separating the ethmoid sinus from the orbit, is frequently the site of continuous infection dissemination to the orbit. At birth, the ethmoid sinus is present.
The connective tissue barrier known as the orbital septum divides the preseptal from the orbital space and continues from the skull into the lid.
Proptosis, globe displacement, orbital apex syndrome (mass influence on the cranial nerves), optic nerve compression, and vision loss are all consequences of cellulitis in the closed bony orbit.
Adult surgical specimen cultures frequently support the growth of several species. In more than one-third of instances, no pathogen is found. In most cases, an organism cannot be grown in blood cultures.
Staphylococcus aureus, Streptococcus pneumoniae, and Streptococcus anginosus are the most prevalent microorganisms.
Less common pathogens include: - Mycobacterium tuberculosis, Eikenella corrodens, Aeromonas hydrophila, Pseudomonas aeruginosa, and rare cases of orbital cellulitis caused by non-sporeforming anaerobes. (3) - In immunocompromised patients, mucormycosis and aspergillosis should be taken into consideration as potential causes of orbital cellulitis. MRSA is becoming more and more important.
Genetics
No inherited tendency is known

Risk Elements 

There is sinusitis in 80–100% of cases. Adults are frequently affected with pansinusitis.

 History of sinus surgery, ophthalmic surgery, retained orbital foreign body (FB), and/or orbital trauma

Immunosuppressed patients are more likely to experience negative effects from dental, periorbital, cutaneous, or cerebral infections, as well as acute dacryocystitis (inflammation of the lacrimal sac) and acute dacryoadenitis (inflammation of the lacrimal gland).


Prevention measures include avoiding trauma to the sinus and orbital areas, receiving routine Hib vaccinations, treating bacterial sinusitis appropriately, and providing proper wound care and perioperative monitoring of orbital surgery and trauma.

Accompanying Conditions 

Adverse outcomes include neurotrophic keratitis, secondary glaucoma, septic uveitis or retinitis, exudative retinal detachment, meningitis, cranial nerve palsies, panophthalmitis, inflammatory or infectious neuritis, orbital abscess, subperiosteal abscess, orbital apex syndrome, subdural or brain abscess, and degenerative optic neuro


Acute red, swollen, sore, and painful eye or eyelid complaints; a history of surgery, trauma, sinus or upper respiratory infections; a tooth infection; and malaise, fever, stiff neck, changes in mental status.
● Proptosis, double vision, ophthalmoplegia, vision loss (or limited field of vision), pain with eye movement, and diminished color vision (differentiating green and red) are specific symptoms of orbital cellulitis.


Caution 
The crucial diagnostic step is to distinguish between orbital and preseptal cellulitis. Examination or a CT scan after it can detect preseptal cellulitis.
A red, swollen, and painful eye or eyelid is the initial symptom of both preseptal and orbital cellulitis.
Ophthalmoplegia, proptosis, diplopia, painful extraocular motions, visual loss, and fever all point to orbital involvement.
The preferred imaging technique when there is a possibility of ocular cellulitis is contrast computed tomography (CT).
Administer urgent IV antibiotics, admit patient to hospital, and refer patient to ophthalmology.
Regularly check for meningitis, abscess, cavernous sinus thrombosis, and vision loss.

clinical assessment 

signals of life

 Check your visual acuity (and wear glasses if necessary).
Examining the lid and feeling the orbit
Afferent pupillary deficiency and the pupillary reflex
Extraocular motions; check for pain when moving your eyes; if it's there, be concerned about orbital cellulitis.
Red desaturation: When a patient compares the color of a red object with that of the other eye, the diminished red color may be an indication of optic nerve involvement.
Proptosis and palpable discomfort
Testing in a confrontational visual field

Differential diagnosis: Preseptal cellulitis, characterized by eyelid erythema, with or without conjunctival erythema, afebrileness, absence of pain with eye movement, absence of diplopia, normal eye examination, and unimpaired vision
In rare instances, metastatic tumors and autoimmune inflammation may mimic orbital cellulitis; these conditions typically have a delayed start of symptoms without discomfort.

After ruling out orbital cellulitis, idiopathic orbital inflammatory illness (orbital pseudotumor) is characterized by afebrile, normal WBCs, is often subacute, may be painful, and responds to drugs.
Arteriovenous fistula (carotid-cavernous fistula) - Orbital FB - spontaneous or brought on by trauma; bruit may be present; subacute, sneaky onset
Cavernous sinus thrombosis: cranial nerves III, IV, V, and VI findings, frequently bilateral and acute - Severely unwell
Acute thyroid orbitopathy, afebrile; potential thyroid disease symptoms; involvement of both orbits
Orbital tumor, unilateral, slow-onset Rhabdomyosarcoma, early lymphoblastic leukemia, or metastatic tumors
Clinical indicators aid in differentiating between preseptal and orbital cellulitis. Examples include trauma, insect bites, and ruptured dermoid cysts. Patients rarely display symptoms of systemic sickness, and preseptal infection causes erythema, induration, and soreness of the eyelid and/or periorbital tissues. It is possible to observe localized skin injuries, abrasions, or bug bites.
Visual clarity and extraocular movements are unharmed.
The eye or eyelid may also be red, puffy, or painful in the case of orbital cellulitis. Proptosis, conjunctival edema, ophthalmoplegia, painful eye movements, and diminished visual acuity are some of the more specific symptoms.

Diagnostic tests and laboratory results

 C-reactive protein differential, ESR, and CBC.
As opposed to preseptal cellulitis, orbital cellulitis can have stronger inflammatory markers.
Although normal flora frequently contaminates swab cultures of eye fluids or nasopharyngeal aspirates, they can still be used to identify the causal organism(s).
At the time of surgery, cultures from sinus and orbital abscesses more frequently produce favorable findings, although they should only be used in situations where invasive operations are necessary.
Multiple organisms may develop in cultures from sinus aspirates and abscesses.
Prior to beginning antibiotic medication in individuals who appear sick or are febrile, blood cultures should be collected (which are typically negative).
Initial examinations (lab, imaging)
The imaging modality of choice is a CT scan of the orbits and sinuses with axial and coronal views, with and without contrast. MRI and US are substitutes.
- Thin section (2 mm) CT, coronal and axial views with bone windows to distinguish preseptal from orbital cellulitis, confirm extension into orbit, identify orbital or subperiosteal abscesses that may need surgery, and discover concurrent sinus disease
- Medial rectus deviation suggests intraorbital involvement.
Although less effective for bone imaging, MRI provides higher soft tissue resolution for detecting cavernous sinus thrombosis.
US is utilized to identify FBs or abscesses, rule out orbital myositis, and track the development of drained abscesses.

Tests in the Future & Special Considerations
Regular eye exams and vital sign checks (every four hours) Identify comorbid illnesses like meningitis or orbital abscesses.

Other/Diagnostic Procedures
Consult an ophthalmologist for a dilated funduscopy and slit lamp examination to determine whether surgery is necessary and to assess proptosis, color vision, and automated visual field.
TREATMENT
Accept individuals with orbital cellulitis for observation and IV broad-spectrum antibiotic therapy.

Medication: Empiric antibiotic therapy for Streptococcus pyogenes, Moraxella catarrhalis, S. pneumoniae, H. influenzae, and other organisms linked to acute sinusitis, as well as for S. aureus, S. anginosus, and anaerobes.
When results for the culture and sensitivity tests are obtained, adjust the IV antibiotic regimen. IV treatment typically lasts a week. Continuation of PO therapy is based on response.
Take into account MRSA therapy for serious infections or depending on regional resistance tendencies.
Patients with severe sinusitis and bone damage are advised to get PO antibiotic therapy for 2 to 3 weeks, or longer (3 to 6 weeks).
Initial Line
If anaerobic infection is suspected, use ampicillin/sulbactam (Unasyn) or ceftriaxone along with metronidazole or clindamycin.
- Ampicillin/sulbactam: 3 g IV every six hours for adults; 200–300 mg/kg/day split every six hours for kids
Clindamycin: 600 mg IV q8h for adults; 20 to 40 mg/kg/day IV q6-8h for children (Ceftriaxone: 1 to 2 g IV q12h for adults; 100 mg/kg/day divided BID in children with a maximum of 4 g/day) (6)
- Metronidazole: 500 mg IV every eight hours for adults; 30 to 35 mg/kg/day divided every eight hours for kids.

Alert

Vancomycin is still the preferred parenteral medication for severe orbital cellulitis and MRSA infection, whether it is suspected or confirmed. Use with other medications to protect against gram-negative bacteria.
Vancomycin: 40 mg/kg/day IV divided every 8 to 12 hours; a maximum daily dose of 2 g for children; 1 g IV q12h for adults.
Next Line
Various antibiotic regimens have been reported to be effective. There isn't a definite agreement on the best option.


Problems to Refer 

Always check with ophthalmology before being admitted to the hospital. If you suspect intracranial spread and have ocular cellulitis, visit ID and ENT as well as neurology or neurosurgery.

Furthermore Treated 
Use of steroids is debatable.
In addition to IV antibiotics, PO steroids may hasten the healing of orbital cellulitis.
Nasal decongestants are frequently advised.
In cases of severe proptosis, topical erythromycin or nonmedicated ophthalmic ointment shields the cornea from exposure.
Amoxicillin/clavulanate can be used to treat adults with 250 to 500 mg TID or children with 20 to 40 mg/kg/day divided doses (9).

Surgical Techniques 
The initial course of treatment is IV antibiotic therapy. In 80–90% of cases, medical treatment works without surgery.

 Complete ophthalmoplegia, a well-defined big abscess (>10 mm) at presentation, or a lack of clinical improvement after 24 to 48 hours of antibiotic therapy all call for surgical surgery.
Trauma instances could require FB removal or débridement.
Surgical drainage may be required for orbital abscess.
The preferred method of treating a brain abscess is surgical drainage followed by 4 to 8 weeks of antibiotics.
External ethmoidectomy, endoscopic ethmoidectomy, uncinectomy, antrostomy, and subperiosteal drainage are among surgical options.

Admission

Patients with orbital cellulitis should be hospitalised for intravenous antibiotics and frequent eye exams to monitor infection progression or optic nerve involvement.
Follow the following parameters: body temperature, WBC, visual acuity, pupillary reflex, ocular motility, and proptosis.
If the condition of an orbital cellulitis patient worsens, a second CT scan or surgical treatment may be necessary.

Patient Follow-Up Monitoring
Serial slit-lamp examinations and visual acuity tests
 

A quick bedside assessment is advised because issues can arise suddenly.

Continuous Action Prevent skin or lid trauma Maintain appropriate hand washing and healthy skin hygiene.

Prognosis 
In the past, before the discovery of antibiotics, 20% of cases resulted in blindness and 17% in death. In 3 to 11% of cases, vision loss occurs.

Vision loss, CNS involvement, and death are complications. Permanent vision loss is caused by corneal exposure, optic neuritis, endophthalmitis, septic uveitis or retinitis, exudative retinal detachment, retinal artery or vein occlusions, globe rupture, orbital compartment syndrome, and CNS complications are caused by intracranial abscess, meningitis, and cavernous sinus thrombosis.

​Kembara Xtra - Medicine- Cellulitis 
Introduction 
With more than 650,000 admissions each year in the United States, skin infections are a significant health burden.
An acute bacterial infection that affects the dermis and subcutaneous tissue.
Orbital cellulitis is an infection of the eye posterior to the septum; sinusitis is the most common risk factor. Periorbital cellulitis is a bacterial infection of the eyelid and surrounding tissues.
- Facial cellulitis: preceded by otitis media or an upper respiratory infection
- Buccal cellulitis: a cheek infection in infants linked to bacteremia that was prevalent prior to receiving the Haemophilus influenzae type B vaccination
Children frequently get peritonsillar cellulitis, which is characterized by fever, sore throat, and "hot potato" speech. Perianal cellulitis is characterized by clearly delineated, brilliant perianal erythema.
- Necrotizing cellulitis: lower extremities infected with germs that produce gas; more prevalent in diabetics

Incidence and Prevalence in Epidemiology 
Males predominate over females. Seasonality hospitalizations for cellulitis are more common in the summer and less common in the winter. 
Incidence
 In 2015, there were 27 annual visits per 1,000 persons for purulent SSTI; 200/100,000 patient years ranged from 0.2 to 24.6 visits per 1000 people per year.
Prevalence
Purulent skin and soft tissue infection (SSTI) visits to U.S. ambulatory offices ranging from 5.4 to 11.35 million visits annually (1); 3.3 million new cases in the country in 2012 costing $15 billion.

Pathophysiology 
Bacterial invasion occurs when the skin's outermost layer, or epidermis, is breached, leading to cellulitis.
Biology, micro
The most prevalent pathogens are gram-negative aerobic bacilli, Staphylococcus aureus, including MRSA, and hemolytic streptococci (groups A, B, C, G, and F).
S. aureus and Pseudomonas aeruginosa are both seen in patients with periorbital and orbital cellulitis and IV drug users, respectively.
- Buccal cellulitis is caused by H. influenza.
- Necrotizing cellulitis caused by clostridium and non-spore-forming anaerobes (crepitant/gangrenous)
- Cellulitis caused by Streptococcus agalactiae after lymph node dissection
- Streptococcus iniae: immunocompromised hosts - Pasteurella multocida and Capnocytophaga canimorsus: cellulitis preceded by bites
– Mycobacterium, fungal (syphilis, aspergillosis, mucormycosis)
Genetics
no inherited pattern

Risk factors include: Skin barrier disruption from trauma, infection, bug bites, drug injections, body piercing, and maceration Inflammation from radiation therapy or excoriating skin conditions Edema from venous insufficiency; lymphatic obstruction from surgery or congestive heart failure (CHF)
Age, diabetes, hypertension, obesity, tinnitus, prior cellulitis, and recurrent cellulitis are all risk factors for the infection.
- Cellulitis recurrence score (predicts recurrence of lower extremity cellulitis based on presence of lymphedema, chronic venous insufficiency, peripheral vascular disease, and deep venous thrombosis) - Recurrent cellulitis is seen in immunocompromised patients (HIV/AIDS), steroids and TNF-α inhibitor therapy, diabetes, hypertension, cancer, peripheral arterial or venous diseases, chronic kidney disease, dialysis, IV or SC drug use.


Prevention measures include elevating the affected area, wearing compression socks, and using pneumatic pressure pumps to reduce edema. Diabetic patients should also maintain glycemic control and take good care of their feet.


Accompanying Conditions 
Obesity, venous insufficiency, lymphedema, and abscess

Diagnosis 

A fast developing unilateral area of erythema, warmth, swelling, and/or discomfort is a sign of the clinical diagnosis.

Providing the Past Portals of entry include prior trauma, surgery, animal or human bites, dermatitis, and fungus infections.
Aching, burning, or itching Chills, fever, and malaise


clinical assessment 
Check vital signs for stability in hemodynamics.
Regional lymphadenopathy, purulent discharge, localized pain and discomfort with erythema, induration, swelling, and warmth.
Proptosis, globe displacement, ocular movement restriction, vision loss, and diplopia are all symptoms of orbital cellulitis.

Malaise, anorexia, vomiting, itchiness, burning, and anterior neck swelling are symptoms of facial cellulitis.

Multiple Diagnoses 
erythema nodosum, sunburn, insect bites, deep vein thrombosis, thrombophlebitis, bursitis, dermatitis, herpes zoster, osteomyelitis, malignancy, and toxic shock syndrome


Diagnostic tests and laboratory results 

Initial examinations (lab, imaging)
Blood cultures, CPK, and CRP should be ordered if there are symptoms of a systemic disease (fever, heart rate greater than 100 beats per minute, or systolic blood pressure less than 90 mm Hg). Think about serum lactate levels.
Plain radiographs, CT scans, and MRIs are helpful in cases of osteomyelitis, fracture, necrotizing fasciitis, and retained foreign bodies. Open wounds should be swabbed for culture.
For assessing any potential underlying abscesses, MRI and ultrasound are the most helpful diagnostic tools.
Procalcitonin is not helpful in the diagnosis of early cellulitis. Gallium-67 scintigraphy aids in the detection of cellulitis superimposed on chronic limb lymphedema.
Other/Diagnostic Procedures
When children with H. influenzae type B or display meningeal symptoms and face cellulitis, lumbar puncture should be considered.

Administration General Therapy 
Sterile saline dressings or cool aluminum acetate compresses for pain alleviation Immobilize/elevate afflicted leg to minimize swelling Edema: compression stockings, pneumatic pumps; diuretic medication for CHF patients 
Mark the erythema's borders to track its development and how well it responds to treatment. If necessary, get a tetanus shot.


The First Line of Medicine
Target treatment for known pathogens and/or specific exposures, such as animal bites
Choosing an empiric antibiotic:
- Cellulitis that isn't purulent
Treatment should concentrate on MSSA and -hemolytic streptococci in cases of nonpurulent discharge.
 Outpatient: treatment lasts 5 to 10 days (5)[C]; studies have indicated that shorter courses of 5 days are equally beneficial as longer courses.
Cephalexin 500 mg PO every six hours (orally) for mild cellulitis; children: 25 to 50 mg/kg/day in three to four doses
Children should take 25 to 50 mg/kg of dicloxacillin four times daily.
Clindamycin 300–450 mg PO every 6–8 hours; for children, 20–30 mg/kg daily in 4 doses
Cefazolin 1 to 2 g IV q8h; children: 100 mg/kg/day IV in 2 to 4 divided doses; Oxacillin 2 g IV q4h; children: 150 to 200 mg/kg/day IV in 4 to 6 doses; IV: for quickly progressive cellulitis
Clindamycin 600 to 900 mg IV every eight hours; children: 25 to 40 mg/kg/day IV in three to four doses; Nafcillin 2 g IV every four hours;
- Purulent cellulitis (likely CA-MRSA): Culture purulent wounds and check back in 48 hours.
Incise abscesses, drain them, and begin empiric antibiotic therapy. Adapt duration based on clinical response; modify based on culture results:
Oral: Trimethoprim-sulfamethoxazole (TMP-SMX) 1 DS pill PO BID; children: dose based on TMP at 8 to 12 mg/kg/day divided in 2 doses; Clindamycin 300 to 450 mg PO; Children: 40 mg/kg/day in 3 to 4 days
Doxycycline 100 mg PO BID; for children older than 8 years old who weigh more than 45 kg, the dosage is 100 mg PO BID.
Linezolid 600 mg PO BID; children 12 years: 10 mg/kg/dose (maximum 600 mg/dose); Minocycline 200 mg PO once and then 100 mg PO BID; Children >8 years: 4 mg/kg PO once and then 4 mg/kg PO BID. 12 years: 600 mg PO BID; PO TID
Tedizolid 200 mg PO once daily; children: No recommended dosage has been determined.
Vancomycin 15 to 20 mg/kg/dose IV every 8 to 12 hours; Daptomycin 4 mg/kg/dose IV once daily; if bacteremia is present or suspected: 6 mg/kg IV once daily; Linezolid 600 mg IV BID; Tedizolid 200 mg IV once daily; Ceftaroline 600 mg IV q12h; Tigecycline 100 mg IV once, then 50 mg IV q12h; Necrotizing cellulitis: requires broad-spectrum
Penicillin plus gentamicin or fluoroquinolones are penicillinase-resistant medications for fresh water exposure; doxycycline 200 mg IV in two separate doses is a medication for salt water exposure.
Bites: Amoxicillin and clavulanic acid are suggested treatments for both human and canine bites. For animal or human bites, the combination of ticarcillin and clavulanic acid or a third-generation cephalosporin (such as ceftriaxone) with metronidazole is an appropriate parenteral therapy. Use fluoroquinolone along with metronidazole if you are allergic to penicillin.
Ceftriaxone IV for adult facial cellulitis

 Cephalexin, cephalexin plus doxycycline, or TMP-SMX plus amoxicillin clavulanate are all effective treatments for mild-to-moderate diabetic foot infections.
- Severe: combinations of antibiotics that target both gram-positive and gram-negative aerobes as well as anaerobes, such as ampicillin-sulbactam, imipenem-cilastatin, or meropenem; alternatively
Admit for empiric antibiotic therapy covering MRSA if there are signs of serious infection, toxicity, immunocompromised patients, or worsening illness despite empirical therapy.
Recurrent streptococcal cellulitis: penicillin 250 mg BID, or erythromycin 250 mg BID if penicillin allergy.
Dalbavancin, a second-generation lipoglycopeptide antibiotic that covers MRSA, can be used to treat cellulitis and is only needed to be taken once a week.
Child Safety Considerations

The Melbourne ASSET tool is useful in detecting the requirement for IV antibiotics in pediatric populations (sensitivity 60%, specificity 93%). Avoid doxycycline in children under the age of 8 and during pregnancy.

Erythromycin 500 mg PO every six hours in the event of a mild illness and a penicillin allergy.

Débridement for gas and pustular materials is one surgical procedure. Cellulitis of the head or neck may require intubation or tracheotomy.

Admission Marked systemic toxicity or worsening symptoms that do not go away after 24 to 48 hours of therapy Patients with underlying risk factors or severe comorbidities Patients with severe infection, tissue necrosis, or severe pain

Patient Follow-Up Monitoring
If the patient remains toxic or not improving, repeat the pertinent blood tests. Symptomatic improvement often happens in 24 to 48 hours, but visual improvement may take 72 hours.

dietary intake 
Sugar regulation in diabetics

Other
Excellent  skin care

In patients with recurrent cellulitis, low-dose penicillin prophylaxis reduces recurrence.

It has been demonstrated that older age, higher BMI, and diabetes mellitus reduce the early response to antibiotics.

Complications include bacterial meningitis, gangrene, local abscess, bacteremia, sepsis, superinfection with gram-negative organisms, lymphangitis, thrombophlebitis or venous thrombosis, and sepsis.

​Kembara Xtra - Medicine- Celiac Disease
Introduction
​A genetically predisposed person's immune system reacts to dietary gluten (present in wheat, barley, and rye), mostly damaging the small intestine. Gliadin, an ingredient in wheat, rye, and barley that is part of the gluten family, is intolerable to those who are affected.
Presentations - Common
 Gluten-free diet (GFD) cures diarrheal disease characterized by villous atrophy and signs of malabsorption (steatorrhea, weight loss, vitamin deficiencies, anemia).
Adults with gastrointestinal (GI) symptoms are 50% of the population.
- Unusual
 Minor gastrointestinal symptoms with a wide range of extraintestinal manifestations (such as anemia, LFTs, dental enamel abnormalities, neurologic problems, and infertility), etc.
- An asymptomatic (quiet) illness
 Discovered during a first-degree relative screening
 Positive genetic tests and lab results; no symptoms or indications; normal histology on biopsy
Systems impacted:
Synonym(s): gluten-sensitive enteropathy; celiac sprue

Incidence and prevalence in epidemiology 

Predominant sex: female > male (3:2); incidence: 1 to 13/100,000 worldwide; 6.5/100,000 in the United States; primarily affects people of Northern European descent.
Approximately 3 million Americans are thought to have celiac disease, with a prevalence of 0.7% in the country and a global prevalence of 1%.

Pathophysiology 

Intolerance to gluten, particularly the gliadin protein component.
GI symptoms and malabsorption follow the alteration of the gliadin protein by tissue transglutaminase (tTG), which causes immunologic cross-reactivity, inflammation, and tissue destruction (villous atrophy).


Genetic homogeneity for HLA-DQ2/DQ8 raises the risk of enteropathy-associated T-cell lymphoma and celiac disease.


First-degree relatives have a 5-20% incidence, but second-degree relatives have a higher risk.
Child Safety Considerations
Other risk factors, including as the processing of grains, genetically modified organisms, poor hygiene and childhood illnesses, breastfeeding, the introduction of solid foods at a young age, pollution, tobacco use, and medicine, do not explain why some people who are vulnerable to the disease have celiac disease while others do not.

Accompanying Conditions  
85% of people with dermatitis herpetiformis (DH) also have celiac disease. Every patient should adhere to GFD.

Osteopenia and osteoporosis, secondary lactase insufficiency, and Hashimoto thyroiditis are among the conditions.
In people with type 1 diabetes, celiac disease affects 3–10% of them.
10-15% of people with symptomatic iron insufficiency have celiac disease.

 Hyposplenism Elevated AST and ALT (without a known cause)
Apthous ulcers of the mouth
 Restless leg syndrome (RLS) Irritable bowel syndrome (IBS)
The risk of small bowel adenocarcinoma and lymphoma is raised in people with celiac disease.
– The histology of the small intestine influences the risk of lymphoproliferative cancers.
– Latent celiac disease (seropositive but normal biopsy) has little to no elevated risk.
Type 1 diabetes, autoimmune thyroiditis, primary biliary cirrhosis, autoimmune hepatitis, psoriasis, and Sjögren's syndrome are associated autoimmune illnesses. Down syndrome, IgA deficiency, Turner syndrome, and Williams syndrome are associated genetic conditions.

Considerations for Pregnancy Up to 19% of men with celiac disease have androgen resistance The prevalence of celiac disease is 2.5 to 3.5 times greater in women with unexplained infertility. With GFD, sperm quality and conception chances improve.
 Increased rates of stillbirths, intrauterine growth restriction, spontaneous abortions, low birth weight, and preterm
Child Safety Considerations
Type 1 diabetes, Down syndrome, Turner syndrome, Williams syndrome, IgA deficiency, and autoimmune thyroid disease are all more common in children with celiac disease.

Diagnosis The most typical GI symptoms are diarrhea and cramping, but other signs and symptoms might also include steatorrhea (fatty stools), abdominal pain or distension, nausea, vomiting, and flatulence, as well as weight loss, weakness, and weariness.
Delay in puberty, iron deficiency anemia, recurrent aphthous stomatitis, dental enamel hyperplasia, headaches, anorexia, and encopresis are some of the clinical symptoms.
Malabsorption in children may show up as chronic lethargy, small stature, or inability to thrive.


clinical assessment 
Physical examinations are frequently typical. 
Orthostatic hypotension and peripheral edema are some of the findings.
Skin: dermatitis herpetiformis (symmetric erythematous papules and blisters on elbows, knees, buttocks, and back), symptoms of anemia. Oropharynx: aphthous stomatitis, glossitis, cheilosis.

Differential Diagnosis for the Abdomen
Short bowel syndrome, small intestinal bacterial overgrowth, lactose intolerance, dyspepsia, gastroesophageal reflux disease (GERD), Crohn disease, Whipple disease, tropical sprue, hypogammaglobulinemia, intestinal gluten sensitivity, type II allergic reaction to gluten with anaphylaxis, non-celiac gluten sensitivity, and intestinal gluten sensitivity.

Findings from the Laboratory and Diagnostic Test 
The gold standard for diagnosis is a tissue biopsy.
Initial examinations (lab, imaging)
When diagnosing adults, do not rely entirely on serology.
While on a gluten-containing diet, patients with symptoms strongly suggestive of celiac disease or those with positive serologies should have an endoscopy for a small bowel biopsy.
During a regular upper endoscopy, a biopsy and histologic study of the duodenal bulb improve the likelihood of diagnosing celiac disease. It is advised to sample the distal duodenum and the duodenal bulb to help histologically confirm the presence of celiac disease.
The preferred serologic test for patients older than two years is IgA anti-tTG.
Total serum IgA can be used as a test for IgA deficiency.
ALERT
If on a regular (non-gluten-free) diet for at least four weeks, positive IgA tTG has a high sensitivity and specificity (sensitivity, 95-98%; specificity, 95%).
Patients with IgA deficiencies have IgA anti-tTG antibodies that are falsely negative.
IgA deficiency is 10–15 times more common in celiac disease patients.
The deamidated gliadin peptide [DGP] antibody is not favoured over the tTG antibody test.

Tests in the Future & Special Considerations
Follow up with anti-DGP IgA and IgG if the patient has an IgA deficiency or if IgA anti-tTG results are negative.
- Anti-tTG has a 94% sensitivity and a 99% specificity.
Use of HLA DQ serotyping for first diagnosis should be avoided.
Think about whether inconsistent serology-histology prevents patients from testing on Down syndrome and GFD patients.
 If osteopenia or osteoporosis is detected during the initial testing but the patient is still exhibiting symptoms or is not adhering to the recommended diet, consider bone mineral density testing at the time of diagnosis and again after a year or two.
The likelihood of achieving mucosal healing increases with younger age at diagnosis, less severe initial histologic damage, and male gender.
Family members are more at risk if there are multiple CD sufferers. Verify your family, including any second-degree relatives. 

Child Safety Considerations
Children experiencing symptoms should be tested for IgA and IgA antitTG antibodies.
IgA anti-tTG Ab monitoring can be used to measure dietary compliance on a regular basis.
Negative serology does not eliminate CD.
For high-risk kids with negative serology, take HLA into consideration.
Limit the use of IgA antiendomysial antibodies in individuals with conditions such type I diabetes or autoimmune liver disease that raise false-positive tTG Ab levels.
Other/Diagnostic Procedures
 At the time of initial evaluation, endoscopy with a minimum of four distal duodenal biopsies and two duodenal bulb biopsies accurately diagnoses 95% of children.

With a sensitivity and specificity between 80% and 95%, video capsule endoscopy is a viable option. It is especially useful if antibody screening and the clinical presentation are consistent with celiac disease despite nondiagnostic duodenal biopsies.
Interpretation of Tests
intestinal biopsy
Plasma cell infiltration, villous atrophy, hyperplasia and extension of crypts, and intraepithelial lymphocytosis in lamina propria
Villous atrophy is additionally brought on by Giardia, Crohn's illness, radiation enteritis, and other food intolerances.

Management and Therapy 
A gluten-free diet (GFD) entails avoiding rye, barley, and wheat.
- Rice, corn, and nut flour are acceptable and secure alternatives.
Uncontaminated oats, rice, corn, tapioca, quinoa, amaranth, and sorghum are among the grains.
The immunological response to gluten will return with the resumption of gluten consumption; levels of IgA antigliadin normalize with gluten abstinence.

First Line of Medicine 

In general, no drugs. Primary treatment is GFD.

Second Line In cases of refractory disease, speak with a GI to discuss the selection, administration, and duration of second-line agents:
- Steroids (budesonide or prednisone) 
- Azathioprine (use with caution; lymphoma risk with usage) Depending on the severity of the disease, individuals may experience nutritional deficiencies that call for adequate supplementation.

Factors for Referral Include Refractory Celiac Disease, Additional Nutritional Support with a Qualified Dietitian, and Children with Positive Celiac Serology.


Healthcare Alternatives 
Numerous alternative treatments are being developed.
Future therapies might involve tight junction blockage, transglutaminase 2 or HLA DQ2/DQ8 blockers, predigestion of gluten using peptidase, or immunological tolerance induction.

Patients who have celiac disease are more likely to get pneumococcal infection. Particularly for people who may not have gotten a pneumococcal vaccination between the ages of 15 and 64, pneumococcal vaccination should be taken into consideration.


Follow-up: Screen for osteoporosis and treat as necessary; consultation with licensed dietician.
If necessary, repeat biopsies should be performed after 12 months and at 3 to 6 months for serology.


patient observation

If there is no clinical response to GFD or a symptom return, repeat the EGD.

Instead of antigliadin IgA or IgG, use anti-tTG IgA or deaminated antigliadin antibodies to gauge dietary response and compliance.


Caution
Eliminate any products containing gluten, including those made from wheat, rye, barley, and processed meat, pharmaceuticals, and personal care items.
Dietary change is difficult (particularly when trying to discover sources of "hidden" gluten), thus it is best to work with a qualified registered dietitian to make it happen.
 Highlight the issues and results of not adhering to a GFD; talk about how to identify gluten in various goods. Support groups and self-education



Prognosis: If you follow the GFD, your prognosis is good.
Patients should feel better within 7 days of changing their diet.
Usually, symptoms go away in 4 to 6 weeks.
It is unknown if rigorous dietary observance lowers the risk of developing cancer.

Complications 
Malignancy: Patients who are untreated or resistant to therapy have a higher risk of developing cancer, but successful treatment lowers that risk to the population average.
Refractory illness, which affects just 1% to 2% of people,
Prednisone may be effective; whole parenteral feeding may be required.
Osteoporosis, electrolyte depletion, dehydration, and vitamin deficiency

​Kembara Xtra - Medicine- Cataract
Introduction 
Any localized or widespread opacity or discoloration of the lens is referred to as a cataract; however, the term is typically only used to describe alterations that impair visual acuity.
 Etymology: called from the opaque frothy look; from Latin catarractes, meaning "waterfall"
Estimated 20 million individuals globally suffer from the leading cause of blindness.
The following types are among them:
- Age-related: 90% of cases are connected to age.
- Metabolic (Wilson disease, hypocalcemia, and diabetes with an accelerated sorbitol pathway)
- Congenital (10-38% of childhood blindness; 1 in 250 infants)
- Myotonic dystrophy and atopic dermatitis (AD) are systemic diseases that are connected.
- Secondary to an ocular condition that is considered to be difficult, such as uveitis linked to sarcoidosis or juvenile rheumatoid arthritis or tumors like melanoma or retinoblastoma.
Traumatic (such as heat, electric shock, radiation, concussion, injuries to the eye that perforate it, and intraocular foreign bodies)
- Nutritional/toxic (such as corticosteroids)
Morphologically speaking:
Because of the increasing refractive index of the lens, nuclear aging of the central lens nucleus is commonly related with myopia. As a result, some elderly individuals may once again be able to read without glasses, a condition known as "second sight."
- Radial, spoke-like opacities; cortical: outer part of lens; may involve anterior, posterior, or equatorial cortex.
- Subcapsular: Posterior subcapsular cataract affects vision more severely than nuclear or cortical cataract; patients with miosis are particularly troubled; near vision is typically more severely impacted than distance vision System(s) affected: elderly Geriatric Considerations tense
All persons over the age of 70 should expect to develop cataracts to some extent.

Child Safety Considerations
Leukocoria may be a possible presenting symptom Pregnancy considerations (including drugs, metabolic dysfunction, intrauterine infection, and malnutrition)

Incidence and prevalence in Epidemiology

Incidence

Cataracts are to blame for 48% of the 37 million cases of blindness that exist worldwide.
 The primary factor contributing to curable blindness and visual loss in underdeveloped nations 
 Predominant age: varies with cataract type

Prevalence
Based on the demographics of the population, cataract prevalence and kind might vary greatly.
Age-related cataract is thought to affect 50% of those aged 65 to 74 and 70% of people over 75.

Pathophysiology and Etiology 

cataract caused by aging:
- As layers of lens fibers are continuously added throughout the course of a person's life, a hard, dehydrated lens nucleus that affects vision is created (nuclear cataract).
- As we age, the biochemical and osmotic equilibrium that is necessary for lens clarity is altered; as a result, the outer layers of the lens hydrate and become opaque, impairing vision.
• Congenital
- Usually no known cause
- Drugs (sulfonamides, corticosteroids in the first trimester)
- Metabolic (mom has diabetes, fetus has galactosemia)
- An intrauterine infection in the first trimester, such as rubella, herpes, or the measles
- Undernutrition in mothers
Other varieties of cataracts
- A biochemical/osmotic imbalance that impairs lens clarity is a common symptom.
- Local variations in the distribution of lens proteins cause light dispersion (lens opacity).

Genetics Congenital (such as chromosomal problems [Down syndrome]) Although the genetics of age-related cataracts is still unknown, it is likely to be a multifactorial issue.

Risk factors include aging, smoking, exposure to UV rays from the sun, diabetes, prolonged use of high-dose steroids, having a healthy family history, and alcohol.


Protection through high-dose, long-term steroid use (systemic therapy > inhaled treatment) Care with UV protective eyewear Avoidance of tobacco products Effective control of diabetes Protective methods using pharmaceutical intervention (e.g., antioxidants, acetylsalicylic acid [ASA], hormone replacement therapy [HRT]) show no proven benefit to date.


Accompanying Conditions 
Diabetes, particularly when there is inadequate glucose regulation
Myotonic dystrophy (visually harmless alteration in 90% of patients in third decade; becomes debilitating in fifth decade)
AD (cataracts commonly develop bilaterally in the second to fourth decades in 10% of persons with severe AD)

Type 2 Neurofibromatosis
Associated ocular disease, or "secondary cataract" (e.g., high myopia, acute [or recurrent] angle-closure glaucoma, chronic anterior uveitis); drug-induced (e.g., steroids, chlorpromazine);
The trauma

Introducing History 

cataract caused by aging:
- Issues with visual acuity in any lighting situation - Falls or accidents; injuries (such as a hip fracture) - Reduced visual acuity, fuzzy vision, distortion, or "ghosting" of pictures
Congenital cataracts are frequently asymptomatic; parents observe their child's strabismus or visual inattentiveness.
- May also have diminished optical acuity
- The proper clinical history or symptoms to aid in diagnosis

clinical assessment 

Assessment of visual acuity for all cataracts - Glare testing enables further evaluation of visual impairment.
Age-related cataract: opacity of the lens during an eye exam
Congenital conditions include: - Lens opacity that develops within three months of birth or at birth; - Leukocoria (white pupil); - Strabismus; - Nystagmus; - Signs of an Associated Syndrome (such as with Down or Rubella Syndrome);
Note: It is important to rule out ocular tumors at all times; retinoblastoma can be treated and diagnosed early for a chance at survival.
 In cases of other types of cataract, physical characteristics (such as metabolic or trauma) may be accompanied by a loss in visual acuity.


Multiple Diagnoses 
An opaque-appearing eye may be caused by malignancy, lens opacities, retinal detachment, or opacities of the cornea (such as scarring, edema, or calcification). A diagnosis should be made via a meticulous ophthalmoscopic examination or a biomicroscopic examination (slit lamp).

The loss of vision in the elderly is frequently caused by a combination of events, including cataract and macular degeneration.
Congenital lens opacity in the absence of other ocular pathology may induce severe amblyopia. Age-related cataract is relevant if symptoms and an ophthalmic exam confirm cataract as a main cause of vision impairment. Relative afferent pupillary response defects are not caused by cataract. abnormal pupillary responses necessitate additional testing to rule out other pathologies.

Diagnostic tests and laboratory results 
Evaluation of visual quality may include tests for glare and contrast sensitivity.
Potential acuity meter testing for the assessment of retinal/macular function
The underlying process's workup

Interpretation of Tests
Although consistent with the type of cataract detected, the diagnosis is made by a clinical examination.


The United States performs 1.64 million cataract extractions each year as an outpatient procedure. 
UV radiation protection for the eyes


There are currently no drugs available to stop or slow the development of cataracts.

Motives for the Referral 
A second evaluation from another ophthalmologist may be necessary if the patient has cataracts and the symptoms do not appear to support the suggestion for surgery.

Surgical Procedures Age-related Cataract: - Surgical removal is required if symptoms of vision impairment are upsetting to the patient, obstructing lifestyle or employment, or creating a fall or injury risk.
– Significant cataracts may grow gradually, making it possible for the patient to be unaware of how it has altered their way of life. The patient says there are "no problems," but the doctor may notice a large cataract. Therefore, evaluation calls for a strong doctor-patient interaction.
– by the primary care physician, before surgery:
Patients taking anticoagulants may need to temporarily stop taking them 1 to 2 weeks prior to surgery, if possible (though this is typically not essential; talk to your ophthalmologist about this).

Patients should inform their ophthalmologist if they have ever used a -blocker, such as tamsulosin (Flomax), as there is an increased risk of developing intraoperative floppy iris syndrome (IFIS), even in those who no longer use these medications.
- Anesthesia: often topical with sedation and vital signs monitoring, although occasionally local injection is also used.
- Surgical procedure: cataract extraction using phacoemulsification through minute incisions made with a blade or laser, followed by implantation of a prosthetic intraocular lens. The power of the intraocular lenses is calculated based on the size of the eye and the curvature of the cornea, and is typically used to correct for distance vision.

Laser-assisted cataract surgery: Using a laser, certain cataract surgery procedures can be completed automatically, including making incisions, releasing the lens capsule, and shattering the cataract before phacoemulsification is used to remove it surgically.
- After surgery, patients often receive a protective eye shield as instructed, a topical antibiotic, NSAIDs, and steroid eye medicines; they should also refrain from lifting or bending for at least a week. generally protecting the eyes.
Surgery is used to remove the cataract in cases with congenital cataracts. Surgery may be necessary for newborns within a few days to lessen the chance of severe amblyopia. Because eyes are developing, the use of lens implants is debatable.
- Postoperative care: hard for the doctor and parents; refractive correction of the operated eye, with frequent follow-up exams; long-term patching regimen for the good eye to counteract amblyopia

Patient Follow-Up Monitoring
The prescription for glasses or contact lenses may alter as the cataract develops in order to preserve vision. Surgery is necessary when this is no longer effective and interferes with the patient's everyday activities.
To improve near and/or far visual acuity after surgery, spectacle correction may still be necessary.
Several weeks after surgery, refraction is frequently advised.


If there are no past or concurrent ocular diseases, the prognosis for removing a cataract is good: 94.3% of otherwise healthy eyes attain best-corrected visual acuity of 20/40 or better. Success rates are decreased when conditions like diabetes and glaucoma are present.

After cataract surgery, posterior capsular opacification can develop and lead to a reduction in vision (14.7–42.7% of eyes, often treated with Nd:YAG laser capsulotomy in the office at a rate of 4–25.3%).
The prognosis for congenital cataracts is frequently worse due to the significant probability of amblyopia.


Complications might range from delayed visual recovery or ongoing eye pain to blindness and eye loss.
In general, complications are rare (2% of eyes).
Poor preoperative visual acuity is associated with surgical difficulties. A posterior capsular rupture is notable among the consequences since it may necessitate additional measures during surgery.

​Kembara Xtra - Medicine- Carpal Tunnel Syndrome 
Introduction 
Median nerve compression neuropathy symptoms
The median nerve is compressed as a result of increased pressure in the carpal tunnel, which causes the recognizable motor-sensory symptoms.
The carpal bones make up the dorsal portion of the carpal tunnel. The palmar boundary is defined by the transverse carpal ligament. - The median nerve and nine flexor tendons are both located in the carpal tunnel.
The dominant hand is typically affected by symptoms, and more than 50% of individuals will have both bilateral symptoms.
Nervous and musculoskeletal systems are both affected


Precaution - Increased incidence (20–45%) during pregnancy
Chronic hemodialysis has a higher incidence (2–31%)

Prevalence and incidence of disease 

 Male > female (3:1 to 10:1) Predominant age range: 40 to 60 years
Incidence
There are two peaks in incidence: late 50s for women and late 70s for both genders. Up to 276/100,000 cases have been observed.

With age, incidence rises.
Prevalence
50 cases per 1,000 people per year in the United States, 4% in women and 2% in males; 14% in patients with diabetes without neuropathy and 30% in patients with diabetic neuropathy.
Increasing lifespan and rising diabetes prevalence may be the causes of the rising prevalence.
Carpal tunnel release (CTR) is one of the most popular hand/wrist treatments, with about 600,000 CTR procedures performed annually. It is also the most expensive upper extremity musculoskeletal disease, costing over $2 billion annually.
The average amount of time American workers with CTS miss is 28 days.

Pathophysiology and Etiology
The median nerve in the carpal tunnel suffers from a combination of mechanical damage, inflammation, elevated pressure, and ischemia injury.
Distal radius fractures and volar lunate dislocations increase risk for acute CTS, which is characterized by fast and prolonged pressure in the carpal tunnel, frequently related to trauma. Chronic CTS is categorized into four categories:
- Idiopathic: edema and fibrous hypertrophy combined but no inflammation
- Anatomical: space-occupying lesion in the carpal tunnel, infection, ganglion cyst, persisting median artery
- Systemic: linked to illnesses like renal failure, amyloidosis, scleroderma, hypothyroidism, obesity, diabetes, and hypothyroidism
- Exertional: repeated palmar impact, repeated use of vibratory equipment, repetitive use of hands and wrists

Unknown genetics; however, a family type has been documented; higher risk of developing CTS if a first-degree relative has the condition.


Risk Elements 

 Extended wrist flexion and extension postures from sports like tennis, cycling, or gardening; recurrent vibration exposure from motorcycle riding — There is inadequate data to link computer use to the onset of CTS.
– Vibratory tool use, food processing and packing, dairy and poultry workers, and assembly workers are the occupations most at risk for CTS. Alterations of fluid balance include pregnancy, rheumatoid arthritis, obesity, renal failure, hypothyroidism, congestive heart failure, and hemodialysis. CTS is the most common neuropathy in people with rheumatoid arthritis.
Neuropathic variables are more prevalent in patients who also suffer from concurrent migraine headaches, including diabetes, alcoholism, vitamin deficiencies, and exposure to pollutants.


Prevention
CTS has no known preventative measures. When performing repetitive tasks requiring the hands or when being exposed to vibratory instruments for an extended period of time at work, it is advised to occasionally (e.g., hourly) take breaks. Losing weight is thought to help prevent CTS.

Diabetes, obesity, pregnancy, hypothyroidism, osteoarthritis of the minor joints of the hand and wrist, hyperparathyroidism, hypocalcemia, and hemodialysis are associated conditions.


Signs and Symptoms 
Nighttime discomfort, numbness, and tingling in the thumb, index, long, and radial portions of the ring fingers; patients may not be able to pinpoint the exact location and may instead experience pain throughout the entire hand.
Early in the disease, hand weakness when performing duties like opening jars is frequently observed.
Paresthesias in the radial digits are a characteristic of the abnormal presentation, and pain may radiate proximally down the median nerve to the elbow and occasionally the shoulder.
 The "Flick sign" is a common way to ease symptoms by rubbing or shaking the hands.
During waking hours, symptoms happen while driving, speaking on the phone, and sometimes when performing repeated hand motions.
The existence of risk factors, such as pregnancy, rheumatoid arthritis, diabetes, chronic hemodialysis, obesity, acromegaly, or occupational exposure


clinical assessment 
Durkan compression test (87% sensitivity, 90% specificity): Direct compression of the median nerve at the carpal tunnel for 30 seconds causes symptoms.
Positive Phalen sign: Paresthesias, numbness, or pain are triggered when the wrist is fully extended for 60 seconds (68% sensitivity, 73% specificity).
Positive Tinel sign (50% sensitivity, 77% specificity): Tapping across the palmar surface of the wrist close to the carpal tunnel may result in an electric feeling along the median nerve's distribution.
Square-sign test: Positive if wrist width/height measurement is more than 0.7 (53 percent sensitivity, 80 percent specificity)
The thenar musculature loss is a late symptom and shouldn't be utilized to rule out CTS (16% sensitivity, 94% specificity). Loss of two-point discriminating. Reduced pain sensitivity.


Multiple Diagnoses 

 Cervical spondylosis (sometimes known as "double crush"); carpal tunnel syndrome may also accompany cervical spine illness.
Upper trunk brachial plexopathy and generalized peripheral neuropathy
CNS conditions (such as cerebral infarction and multiple sclerosis)
Anterior interosseous syndrome Ulnar nerve compression Musculoskeletal problems of the wrist Thoracic outlet syndrome Pronator syndrome (median nerve compression at the elbow) 
- Degenerative joint disease - Distal radius fracture from trauma
- De Quervain tenosynovitis - Ganglion cyst - Rheumatoid arthritis - Scleroderma

Diagnostic tests and laboratory results 

The CTS-6, the Kamath and Stothard questionnaire, and the Katz and Stirrat hand symptom diagram are the most accurate screening tools.
No laboratory test can provide a diagnosis.
- Normal serum chemistries, HbA1c, ESR, and thyrotropin (thyroid-stimulating hormone [TSH]) levels can rule out secondary diseases linked to CTS.

Specialized examinations - Electrodiagnostic studies
85% sensitivity and 95% specificity
Most effective when there is a low pretest probability and a suspicion of radiculopathy, alternative peripheral neuropathy, or the "double-crush" syndrome, which involves compression in numerous places.
Studies on nerve conduction compare the amplitude and delay of median nerve signals traveling through the carpal tunnel.
Median sensory distal delay, which is prolonged in CTS, is the most sensitive sign.
Standard wrist radiographs are not required to diagnose CTS but are used to evaluate the bone structure and degenerative joint condition.
Magnetic resonance imaging offers only marginal advantages over ultrasound, which is a quick, painless, noninvasive modality with 87% sensitivity and 83% specificity and a hypoechoic median nerve cross-sectional area greater than 9 mm.

Control and Prevention 
There is substantial evidence that local steroid (methylprednisolone) injection and immobilization (brace, splint, orthosis) improve patient-reported outcomes.
A trial of nonoperative care is typically advised for individuals with mild to moderate CTS symptoms. Strong data indicates that surgical treatment of CTS results in better functional gains at 1 year compared with nonoperative treatment.
First Line: MEDICATION
Injections of local corticosteroids and night splinting (12 weeks) are standard therapies for mild to moderate CTS.
Recent studies have demonstrated that a single local corticosteroid injection significantly improves outcomes in terms of pain, function, and nocturnal paresthesia remission when compared to night splints at 1-, 3-, and 6-month follow-up.

A favorable reaction to an injection could indicate a better chance that surgery will be beneficial.
The injection's adverse effects on collagen and proteoglycan synthesis, tenocyte activity, and mechanical strength of the tendon all contribute to additional degeneration and rupture risk.
Surgery should be considered for people with resistant or recurring symptoms because there is no evidence to support numerous injection treatments; early surgery is also beneficial for those with moderate to severe condition.

Next Line
Although oral corticosteroids have not been proven to have any long-term advantages, they are more effective than placebo in the short term and less effective than local corticosteroid injection.
– The small possible benefit of symptom relief should be weighed against the long-term dangers of even a brief course of steroids.
Gabapentin has been proven to be successful in treating CTS symptoms.
- 300 mg per day has been demonstrated to be more effective than 100 mg per day with little to no side effects.

Despite being widely utilized, nonsteroidal anti-inflammatory drugs don't significantly reduce symptoms when compared to a placebo.
- Inhibitory conditions: stomach discomfort
Hand treatment has been demonstrated to improve patient function. NSAIDs' GI adverse effects may prevent their usage in some individuals.


Motives for the Referral
Before any surgical operation, electrodiagnostic investigations are typically obtained.


Surgical Techniques 
In >95% of individuals, completely severing the transverse carpal ligament relieves symptoms.
An outpatient technique called surgical decompression is carried out under local or regional anaesthetic.
It typically takes 2 weeks for an incision to heal; a further 2 weeks may be needed before utilizing the affected hand for activities demanding strength.
After 9.3 years of follow-up, 93.8% of patients with severe CTS had completely recovered from their numbness.

The strategy should be determined by the surgeon's and the patient's preferences.
- Endoscopic surgery had a positive impact on patient satisfaction, key pinch strength, time to return to work, and scar-related problems (6)[A].
Patients receiving endoscopic release are more likely to experience temporary nerve damage, but this effect is rarely long-lasting.


Healthcare Alternatives 
The use of vitamin B6 in the prevention or treatment of CTS is not supported by any experimental data.
Acupuncture has been demonstrated to be equally effective as short-term oral prednisolone medication and can be used as an adjuvant or alternative therapy.
There is no evidence to support the use of chiropractic therapy to treat CTS.

Outpatient Admissions


Patient Follow-Up Monitoring
Patients who receive nonoperative treatment (splinting, injections) need to be monitored for 4 to 12 weeks to make sure they are making enough progress.
7-20% of individuals treated surgically may experience recurrence; nevertheless, there is only limited, low-quality evidence to support the benefits of rehabilitation exercises including wrist immobilization, ice therapy, and multimodal hand rehabilitation.

Nutritional 
There is little proof to support claims that a particular diet helps to lower risk or treat CTS symptoms.

Prognosis: Within 4 years, symptoms will return in about 85% of individuals who at first react well to conservative therapy.
Thenar wasting and a positive Phalen test have both been linked to worse outcomes with conservative therapy.
Patients with severe CTS could not make a full recovery following surgery. If untreated, more severe cases of CTS can result in numbness and weakness in the hand, atrophy of the thenar muscles, and permanent loss of median nerve function. Paresthesias and weakness may linger, but nighttime symptoms typically go away.

Postoperative infection, an uncommon complication
Damage to the median nerve or its recurrent (motor) branch Pillar pain, which is discomfort near the real ligament release sites of the trapezial ridge and hook of hamate, in the months following CTR (prevalence of 6-36%)

​Kembara Xtra - Medicine- Carotid Stenosis 
Introduction 
Atherosclerosis is the most frequent origin of carotid stenosis, but it can also result from intimal fibroplasia, vasculitis, adventitial cysts, or vascular malignancies.
The carotid artery lumen usually narrows as a result of atherosclerotic alterations in the vessel wall. 90% of extracranial carotid lesions and up to 30% of all ischemic strokes are caused by atherosclerotic plaques.
● Carotid stenosis that is "hemodynamically significant" causes a drop in pressure or a decrease in flow. It roughly equates to a stenosis with a diameter reduction of 60–99%.
● Following criteria are used to categorize carotid lesions: - Symptomatology
Asymptomatic patients tend to be homogenous and stable, while symptomatic patients are more likely to have strokes or transient ischemic attacks. High grade stenosis ranges from 80 to 99%.
Low grade: 50% stenosis; Moderate grade: 50-79% stenosis


Prevalence and incidence of disease 

more typical among men and as people get older 
Unknown incidence (many asymptomatic patients go undetected.)
Prevalence

Age 50 years: males 0.2%, women 0%; Age >80 years: men 7.5%, women 5%; Moderate stenosis

Age 50 years: men 0.1%, women 0%; severe stenosis
- Age >80 years: 3.1% men, 0.9% women

Pathophysiology and Etiology 
At the carotid bifurcation, atherosclerosis typically starts around adolescence. The carotid bulb's blood flow patterns are distinctive. Endothelial dysfunction and damage are brought on by hemodynamic abnormalities. Stenosis then develops as a result of plaque formation in the vessel wall.
Although the root reason is not fully understood, there are some risk factors that are usually present. The vessel wall's tensile stress, turbulence, and artery wall shear stress appear to be at play.

Genetics – Increased prevalence in families – Genetically connected factors – Obesity, Diabetes mellitus (DM), race, and hypertension (HTN) – TNFSF4, PPARA, TLR4, ITGA2, and HABP2 were all significantly related with worse carotid plaque in a recent single nucleotide polymorphism research.

Risk factors include male sex, family history, advanced age (>65 years old), coronary artery disease (CAD), peripheral artery disease, aortic aneurysmal disease, and congenital arteriopathies. 
Smoking, diet, dyslipidemia, physical inactivity, obesity, HTN, and diabetes are all modifiable variables.
Chlamydia pneumoniae and cytomegalovirus are potential causes. 


Prevention

 Antihypertensive medication to keep blood pressure under 140/90 mm Hg (systolic blood pressure of 150 mm Hg is preferred in older patients).
Quitting smoking to lower the risk of developing atherosclerosis and having a stroke 
Lipid control: statin therapy-induced reduction of carotid atherosclerotic lesions

Stroke and transient ischemic attack (TIA) are associated conditions. 
Peripheral vascular disease (PVD), CAD/myocardial infarction (MI), hypertension, and diabetes mellitus
• Hyperlipidemia


Diagnosis 

It is not advised to perform a carotid stenosis screening.
However, a workup for this condition may be necessary if there are symptoms that point to a stroke or TIA.

History of a cerebral ischemia event, identification of comorbidities that can be managed and those that cannot, identification of strokes, TIAs, amaurosis fugax (monocular blindness), aphasia, and CAD/MI

Review of systems with an emphasis on the risk factors for stroke (HTN and arrhythmias) and peripheral arterial disease

clinical assessment 
Amaurosis fugax causes transitory ipsilateral blindness due to retinal ischemia. Lateralizing neurologic deficits: contralateral motor and/or sensory deficiency. 
Dysarthria, aphasia (in the case of dominant hemisphere involvement, typically left), and visual field deficiency 
Low sensitivity and specificity for carotid bruit

Aortic valve stenosis, aortic arch atherosclerosis, arrhythmia with cardiogenic embolization, migraine, a brain tumor, metabolic abnormalities, a functional or psychological deficiency, and seizures are among the possible diagnoses.

Diagnostic tests and laboratory results 

Initial examinations (lab, imaging)
Workup for TIA/stroke suspicion may involve the following:
With differential, CBC
ESR (in the case that temporal arteritis is a factor) and a basic metabolic panel 
Fasting lipid profile; glucose/hemoglobin A1c
The first diagnostic test that is advised for asymptomatic patients with carotid stenosis that is known or suspected is duplex ultrasonography.
Duplex ultrasonography (US) has an accuracy of 98% and a sensitivity of 88% in detecting 50% of stenosis.

Tests in the Future & Special Considerations
If a history or physical examination suggests stenosis, proceed to imaging. Other noninvasive imaging methods can enhance duplex results. - CT angiography has a 100% specificity and 88% sensitivity.
 Requires MR angiography, which has a 95% sensitivity and 90% specificity, and requires IV contrast with a risk of future kidney morbidity.
 Analyzes the aortic arch, common carotid artery, and cerebral circulation (intra- and extracranial). If any of the following traits are present, unstable plaque is likely present: 
Thin/ruptured fibrous cap is present.
Has a necrotic core rich in lipids and tends to overstate the degree of stenosis

Other/Diagnostic Procedures
The usual gold standard for diagnosis is cerebral angiography: 
Outlines the aortic arch and proximal vessels' anatomical features. 
The procedure is invasive and comes with a number of risks: - Renal impairment brought on by contrast (1–5% complication rate)
Neurologic problems and thromboembolic-related issues (complication rate: 1-2.6%) - Should only be utilized when other tests are inconclusive
Interpretation of Tests
At the carotid bifurcation, stenosis frequently develops, with plaque formation most frequently occurring at the level of the proximal internal carotid artery: Plaque resides in the intima and inner media, avoiding the outer media and adventitia, and is thickest at the carotid bifurcation.

Homogenous (stable) plaques hardly ever bleed or ulcerate, according to plaque histology:
 Deposition of fibrous tissue and fatty streaks
Heterogenous (unstable) plaques may bleed or ulcerate due to diffuse intimal thickening.
 The presence of cholesterol crystals, necrotic debris, and macrophages that are lipid-loaded Ulcerated plaques are soft, gelatinous clots made up of red and white blood cells, platelets, and fibrin.

Management 
The main treatments for both asymptomatic and symptomatic carotid stenosis are quitting smoking, blood pressure management, antiplatelet medicine, and statin medication.

Treatment 

 Patients should be counseled to stop smoking and offered smoking cessation intervention to lower the risk of atherosclerosis development and stroke. Lifestyle modifications: food control and weight loss, exercise of 30 minutes per day at least five days per week.

 Managing HTN with antihypertensive medications to keep blood pressure under 140/90 mm Hg, or 150/90 mm Hg in elderly patients. Tighter blood pressure control may prevent cerebrovascular incidents in carefully chosen individuals, however this is questionable.

Medication: Antihypertensive therapy (140/90 mm Hg or, in the elderly, 150/90 mm Hg 
Exercise, quitting smoking, and a healthy diet are beneficial therapeutic add-ons.
The risk is decreased in people with diabetes when a comprehensive program includes tight management of HTN with ACEI or ARB medication. Statin initiation is advised; consider moderate- to high-intensity statin therapy for anti-inflammatory effect. It is unknown whether rigorous glucose-lowering medication helps prevent strokes.
Aspirin: 75 to 325 mg/day If the patient has a sustained TIA or ischemic stroke, antiplatelet therapy with aspirin alone (75 to 325 mg/day), clopidogrel alone (75 mg/day), or aspirin plus extended-release dipyridamole (25 and 200 mg BID, respectively) is recommended. Combining clopidogrel and aspirin within three months after the TIA or CVA is not advised.

Motives for the Referral 
Order imaging and get in touch with neurology if you have recent stroke symptoms.
If the carotid stenosis is known and the patient is a candidate for surgery, some experts advise duplex imaging every six months.

Carotid endarterectomy (CEA) is of some benefit in patients with 50–69% symptomatic stenosis, highly beneficial for those with 70–99% stenosis without near-occlusion, and ineffective in patients with carotid near-occlusion. Surgical Procedures Symptomatic carotid stenosis (history of ischemia ipsilateral to stenosis) - Patients with a minimum 5-year life expectancy are advised to undergo CEA. Predicted perioperative stroke or death rates must be less than 6%.
– All individuals with CEA are advised to take aspirin (81 to 325 mg/day) as part of their treatment.
Prior to surgery, aspirin should be taken daily for at least three months, but it can be continued permanently.
– Similar long-term results are seen with carotid artery stenting (CAS) as with CEA. When contemplating a carotid intervention, age should be taken into account.
CAS has a similar mortality risk in the young and the elderly, but the elderly have a higher risk of unfavorable cerebrovascular events. In spite of higher mortality, CEA is linked to similar neurologic outcomes in both young and old people.
 In some patients with neck anatomy that is unfavorable for vascular surgery and those with concomitant diseases that significantly raise the risk of anesthesia and surgery, CAS is recommended.
For 30 days following CAS, dual antiplatelet therapy using aspirin (81 to 325 mg/day) and clopidogrel (75 mg/day) is advised.

Patients who have no symptoms: If surgery is offered as a management option for asymptomatic carotid stenosis, CEA is preferable over CAS. Increased risks of periprocedural stroke and periprocedural death are possible with CAS. - With modern medical management, the benefit of surgical therapy over medical therapy has diminished. With the available literature, it is impossible to make an evidence-based recommendation for or against surgical therapy.


Admissions
Any patient exhibiting acute symptoms of carotid stenosis should be admitted to the hospital for additional diagnostic testing and the necessary treatment.
Rapid evaluation for TIA-compatible symptoms should be acquired in an inpatient or emergency department (ED) environment.
Discharge requirements include ambulation, appropriate PO intake, and neurological integrity 24 to 48 hours after CEA.

Patient Follow-Up Monitoring
Duplex every 6 to 12 months; Duplex at 2 to 6 weeks following surgery; Reoperative CEA or CAS is reasonable in cases of fast progressing restenosis.
Patients who have any of the following conditions are at high risk of readmission after CEA: renal failure, heart failure, diabetes, and age >80 years; as a result, comprehensive medical care and stringent follow-up are advised.
A heart-healthy diet without trans fats and low in saturated fat


Complications 

Untreated TIA/stroke: 1.68 percent annual risk of ipsilateral stroke 
Perioperative (within 30 days) - Postoperative (state after CEA)
 MI - Late (>30 days postoperative), cranial nerve damage, bleeding, hemodynamic instability
 False aneurysm and recurrent stenosis at the surgery site

​Kembara Xtra - Medicine- Carotid Sinus Hypersensitivity 
Introduction
The baroreceptors in the carotid sinus are sensitive to changes in artery pressure and are found close to where the internal and external carotid arteries split.
The carotid sinuses are crucial to maintaining the balance of blood pressure (BP).
In carotid sinus hypersensitivity (CSH), stimulation of one or both carotid sinuses, such as mechanical forces with turning neck), causes an exaggerated baroreceptor response that can slow the heart rate and raise blood pressure. An endogenous increase in BP or external pressure applied to a carotid sinus increases the baroreceptor firing rate, activates vagal efferents, and/or inhibits the sympathetic discharge to the heart and blood
● There are three ways to define CSH:
Standard criteria include a 3 second halt in heart rate in response to carotid sinus massage (CSM) and/or a vasodepression of a systolic blood pressure drop of at least 50 mm Hg.
– Krediet criteria: a heart rate halt lasting six seconds in response to CSM and/or a drop in blood pressure to 60 millimeters of mercury for six seconds.
CSH is typically divided into three subtypes based on response to CSM: a pause in heart rate in response to CSM >95th percentile of the population response (7.3 seconds asystole), and/or vasodepression in response to CSM >95th percentile of the population response (>77 mm Hg fall in systolic BP), or both.
- Cardioinhibitory (70–75%): at least three seconds of asystole
- Vasodepressive (5-10%): systolic blood pressure falls by at least 50 mm Hg.
- Mixed (20–25%): the first two categories together.
Carotid sinus syndrome (CSS) is a term that is frequently (though not always) used to describe CSH with syncope and can be categorized as:
Syncope caused by unintentional mechanical manipulation (trigger) of the carotid sinuses, such as shaving, wearing a tight collar, or tumors, is known as spontaneous CSS.
- Induced CSS: CSM diagnoses syncope despite the absence of a mechanical stimulus.


Prevalence and incidence of disease 
Age-related disease that most frequently affects men over 65.
Correlated with a history of hypertension (HTN) and coronary artery disease (CAD), with right CSH prevalence being higher than left CSH
Using accepted diagnostic criteria, CSH was discovered in 39% of randomly chosen adults over the age of 65 in 2006. This finding was compared to a 2019 evaluation of prevalence statistics.

30% of older adults with unexplained syncope may have CSH at the root of their symptoms.

Pathophysiology and Etiology
It is still unclear what specific defect in persons with CSH produces the hypersensitive reaction. This condition may result from modifications to any component of the reflex arc or the target organs, or it may be a symptom of a systemic autonomic illness linked to autonomic dysregulation.
Linked to elevated baroreflex sensitivity and resting sympathetic overactivity
Bradycardia and asystole are thought to be mediated by vagal efferents in the cardioinhibitory and mixed CSH subtypes, whereas vasodilation and arterial hypotension are thought to be caused by a reduction in sympathetic tone in the vasodepressor and mixed subtypes.
Cerebral autoregulation has been linked to symptoms of CSH, and it has been discovered to be normal in asymptomatic CSH.
CSH is typically idiopathic but can be brought on by: - Carotid body tumors - Increased afferent impulse traffic in the baroreflex pathway as a result of atherosclerosis.
- Neck lymph nodes that are inflammatory and cancerous - Significant scarring around the carotid sinus from earlier neck surgeries - Metastatic cancer

Risk factors include advanced age, being a man, and CAD, HTN, and DM.

Vasovagal syncope, sick sinus syndrome, atrioventricular block, coronary artery disease, hypertension in the lower extremities, Alzheimer disease, Parkinson illness

Introducing History
Unexplained falls: Evidence of a causal association between falls and the cardiac inhibitory subtype is proposed. Recurrent syncope: typically sudden, unexplained, of short duration, appearing spontaneous, and with complete recovery.

Dizziness is more commonly associated with vasodepressor and mixed subtypes, and presents as momentary light-headedness or presyncope rather than real vertigo.
Syncope and prodrome or retrograde amnesia may occur together.
Any CSM-like action, such as shaving, donning a tight collar, or turning one's head forcefully, are exacerbating or causative factors. Neck trauma, radical neck resection, severe scarring in the neck from radiation fibrosis, and neck malignancies - There are some drugs that can make CSH symptoms worse:
Digoxin or beta-blockers, particularly those of the cardioinhibitory subtype
Methacholine, morphine, and physostigmine all increase vagal sensitivity and may put someone at risk for the cardiac inhibitory subtype of CSH.

clinical assessment 

Unless the carotid baroreceptor is activated, which causes bradycardia, hypotension, pallor, and diaphoresis, everything is OK.

Differential Diagnosis: Neurocardiogenic Syncope, Postural Hypotension, Situational Syncope, Postural Tachycardia Syndrome (POTS), Primary Autonomic Deficiency, Hypovolemia, Dysrhythmias, Sick Sinus Syndrome, Cerebrovascular Deficiency, Other Causes of Syncope (e.g., Metabolic, Psychogenic), and ECG that may show sinus pauses or atrial-ventricular block.

 Carotid duplex scan to exclude carotid stenosis if there is a bruit (see the one after this one)


Diagnostic tests and laboratory results 
Other/Diagnostic Procedures
After a negative initial evaluation, CSM is recommended for patients >40 years old with syncope of unknown cause. The steps in this technique are widely acknowledged as necessary for effective diagnosis.
- For better diagnostic accuracy, the patient is placed in the supine position for 5 minutes while having their baseline blood pressure and electrocardiogram continuously monitored (on a footplate-style tilt table).
– Apply firm longitudinal massage for 5 to 10 seconds over the right carotid sinus (between the angle of the mandible and the superior border of the thyroid) at the location of the greatest pulsation:
Record symptoms, BP, and record ECG changes. Keep in mind that gentle pressure over the carotid sinus will not consistently result in a hypersensitive reaction.
 Stop if asystole is less than three seconds.
– Apply pressure to the left carotid sinus while the patient is still supine if the initial test is nondiagnostic; if it is still nondiagnostic, repeat the test with a head-up tilt of 70 degrees (first to the right, then, if required, the left), giving the patient time to adjust hemodynamically to the head-up position.
- Supporting data for the testing strategy
First, the right side: 30% of CSM exams are found to be nondiagnostic in the supine position; the positive predictive value increases from 77% to 96% with a specificity of 93% by performing CSM in the 70-degree position. Up to 66% of CSH have positive response on the right; if a positive right response, there is no need to repeat the test on the left side.
Absolute contraindications to CSM testing include the presence of a carotid bruit, which requires initial examination with carotid ultrasonography and Doppler.
No testing if stenosis is greater than 70%, and supine-only testing if stenosis is between 50% and 70%. Myocardial infarction, transient ischemic attack, or stroke within the last three months. History of ventricular tachycardia or ventricular fibrillation is a relative contraindication to CSM testing, and elderly patients are more likely to have false-positive results. It is important to rule out any further syncope reasons.
– There have been reports of neurological and cardiovascular problems during CSM. Cardiovascular issues, in particular arrhythmia, are relatively uncommon. 
Within 0.9% of individuals, transient neurologic symptoms and signs can be present. Following CSM, persistent neurologic impairments are relatively uncommon. CSM should be regarded as a risk-free, safe process when done properly (3)[C].
Interpretation of Tests
Although the standard positive response criteria (asystole 3 seconds and/or a reduction in systolic blood pressure 50 mm Hg) are based on historical observations, a professional analysis of more current data suggests these criteria may be overly sensitive.

If a patient's syncope is replicated during a test, the CSM approach becomes more specific.


Management and Therapy 
In asymptomatic people, isolated CSH doesn't need to be treated.

In patients with vasodepressor subtype and no other cardiovascular disease, high salt consumption and increased fluid intake may be useful to maintain intravascular volume.
Assessment of driving restrictions

The First Line of Medicine
No one medication has proven to be consistently useful in treating recurrent and symptomatic CSH.
Next Line
In patients with vasodepressor subtype, fludrocortisone or midodrine may be used to alleviate orthostatic symptoms (FDA has not cleared this use).
Fludrocortisone, however, promotes salt and water retention and should only be administered with caution in older heart disease patients. The fact that midodrine raises mean ambulatory BP is a side effect.
Atropine may be administered to patients with the cardioinhibitory subtype of bradycardia in the acute context. There is some evidence that sertraline and fluoxetine help people who are not responsive to pacemakers.


Surgical Techniques 
The 2017 ACC/AHA/HRS Guideline for the Evaluation and Management of Patients With Syncope states that the strength of the recommendations is low because the evidence is scarce. The evidence that is currently available does not support the use of pacing for reflex-mediated syncope in individuals other than those who have asystole and recurrent vasovagal syncope as verified by an implantable loop recorder.
Permanent pacing may lessen the frequency of symptoms, but it may not be able to get rid of them entirely.
Surgery for CSH patients due to the bulk effect of the tumor burden

Due to the high likelihood of problems, carotid sinus denervation with surgery or radiation therapy is no longer advised.

Steer clear of triggering actions (as mentioned above) that put strain on the neck, such as wearing a necktie or collar that is too tight.
If you experience syncope, avoid driving or engaging in other potentially risky activities until your doctor gives the all-clear.

 Steer clear of drugs that can cause symptoms to recur, such as vasodilators.
Teach the patient to lie down if prodromal symptoms or presyncope appear.
Describe the diagnosis, offer assurance, and describe the possibility of a recurrence.

Prognosis It has not been established that CSH confers a separate mortality risk.
Patients with untreated CSS have a recurrent risk of syncope as high as 62% in just four years.
In patients with cardiac inhibitory CSH who received pacemakers, the mean number of falls decreased significantly over a 1-year follow-up period, from 9.3 to 4.1.

Complications 

Kerr criterion indicates a link between CSH and higher mortality. To predict future falls, syncope, and the capacity of criteria to identify patients who would benefit from pacing, more research is required.

​Kembara Xtra - Medicine- Cardiomyopathy  
Introduction 
In the absence of coronary artery disease, congenital heart disease, valve disease, or hypertension that could adequately explain the clinical myocardial dysfunction, cardiomyopathies are myocardial disorders that cause structural and functional heart abnormalities.

With the current classification system, it is possible to distinguish between cardiac diseases that are limited to the myocardium (primary) and those that are secondary to systemic problems. A third, distinct category is given to specific causes of myocardial dysfunction brought on by other cardiovascular diseases.
Primary cardiomyopathies are those that primarily affect the myocardium.
The genetic
Cardiomyopathy with hypertrophy (HCM)
Left ventricular (LV) noncompaction (LVNC), arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVC/D), and more
Storage of glycogen (Danon type, PRKAG2)
Conductivity issues
Ion channel diseases, including long QT syndrome (LQTS), Brugada syndrome, short QT syndrome, and catecholaminergic polymorphic ventricular tachycardia (CPVT), include mitochondrial myopathies. Mixed (non-genetic and genetic)
Restrictive (nonhypertrophied and nondilated) dilated cardiomyopathy
Myocarditis, stress cardiomyopathy, peripartum, tachycardia-induced birth defects, and children of type 1 diabetes moms are acquired conditions that are secondary (multiorgan involvement; see list below).
 Particular: congenital heart disease, hypertension, ischemia, and valvular heart disease 

End-stage cardiomyopathy patients have stage D heart failure or significant symptoms at rest that are resistant to conventional medical treatment.
cardiovascular, renal, hepatic, and pulmonary systems are impacted Child Safety Considerations
Early diagnosis and a progressive course may change the course of the disease. causes include endocrine, uremic, nutritional, childhood LVNC, DCM, HCM, and RCM. pregnant women's issues
Peripartum cardiomyopathy (PPCM) can happen months before and after delivery in peripartum women.


Prevalence and incidence of disease 

The most common cause of ischemic cardiomyopathy, which affects people mostly over 50 years old, is aging. Think about unusual reasons in children. HCM is a significant underlying cause of heart failure impairment and the most frequent cause of sudden cardiac death in young people.
Incidence
 DCM: 5–8 new cases per 100,000 people each year.

Prevalence
At least 1 in 500 adults have DCM, which is the third most common cause of heart failure and the most common reason for heart transplantation. Tropical regions are more likely to experience RCM.

Pathophysiology 
LVNC: congenital cardiomyopathies with "spongy" appearance of the LV myocardium; HCM: hypertrophied, nondilated left ventricle; ARVC/D: involves the right ventricle with progressive loss of myocytes and fatty/fibrofatty tissue replacement; can be associated with myocarditis (adenovirus or enterovirus); LQTS: most common ion channelopathy with prolonged ventricular repolarization and QTc RCM is defined as normal/decreased ventricular volume with restrictive physiology, enlarged biatrial chambers, and impaired ventricular filling. Myocarditis is defined as an acute or chronic inflammation of the myocardium caused by toxins, drugs, or infectious causes. PPCM is defined as a form of DCM with LV systolic dysfunction and heart failure of unknown etiology. Stress cardiomyopathies are defined as acute but quickly reversible  Viral infections such as HIV, coxsackievirus, and adenovirus are infectious causes.
- Mycobacterial and bacterial diseases (such as diphtheria and rheumatic fever). - Parasitic (such as trypanosoma cruzi and toxoplasmosis) 
Neuromuscular/neurologic: Duchenne and Emery- Dreifuss muscular dystrophies, Friedreich ataxia, myotonic dystrophy, neurofibromatosis, tuberous sclerosis; Infiltrative: amyloidosis, Gaucher disease, Hurler disease, Hunter disease, Fabry disease; Storage: hemochromatosis; Glycogen storage disease (type II, Pompe); Heavy Metal; Chemic; Neuromuscular/neurologic: Sarcoidosis is an inflammatory condition with granulomatous symptoms. Idiopathic conditions include endomyocardial fibrosis and hypereosinophilic syndrome (Loeffler endocarditis).
Genetics
The most prevalent kind of primary hereditary cardiomyopathy, autosomal dominant HCM, is brought on by many mutations in the genes encoding the contractile proteins of the heart sarcomere. Only one-third of DCM instances have genetic origins; these cases are almost exclusively inherited autosomally dominantly. Along with LQTS and other ion-channel abnormalities, LVNC and ARVC are inherited in an autosomal dominant manner as well.

Risk factors include smoking, physical inactivity, excessive alcohol use, dietary salt, obstructive sleep apnea, diabetes mellitus, hypertension, hyperlipidemia, obesity, coronary artery disease, and chemotherapy.

Prevention 
Limit your intake of salt and water, and measure your daily weight and BP at home.


Presenting History: Right upper quadrant pain or bloating; orthopnea; postprandial dyspnea; dyspnea with activity; paroxysmal nocturnal dyspnea; fatigue; syncope; edema


Tachypnea, Cheyne-Stokes breathing, low pulse pressure, cool extremities, jugular venous distention, bibasilar rales, tachycardia, displaced point of maximum impulse (PMI), S3 gallop, blowing systolic murmur, hepatosplenomegaly, ascites, and edema are all signs of a clinical condition.


Differential diagnoses include anemia, recurrent pulmonary embolism, constrictive pericarditis, severe pulmonary illness, primary pulmonary hypertension, and several advanced types of cancer.


Diagnostic tests and laboratory results 
ECG: indications of a previous Q-wave infarction, atrial fibrillation, interventricular conduction delay, and LV hypertrophy 
Prerenal azotemia Hyponatremia
Blood loss

Mild hyperbilirubinemia; mild elevation of troponin; elevated B-type natriuretic peptide (BNP) or pro-BNP; elevated liver function tests; and elevated uric acid
 
Chest radiograph - Cardiomegaly - Increased vascular markings to the upper lobes - Initial tests (lab, imaging) - ECG - There may or may not be pleural effusions.
Global hypokinesis and four-chamber enlargement are signs of DCM, according to echocardiography.
- Severe LV hypertrophy is seen in HCM.
– A past localized myocardial infarction is indicated by anomalies in the LV's segmental contraction.
Cardiovascular magnetic resonance imaging (cardiac MRI) may be helpful in identifying specific nonischemic cardiomyopathies. Stress myocardial perfusion imaging (MPI) is advised for people who have recently developed LV dysfunction or when ischemia is suspected.

Pulmonary artery catheters may be reasonable in patients with refractory heart failure to help direct care. Diagnostic Procedures/Other Cardiac Catheterization - Helpful to rule out ischemic heart disease - Characterize hemodynamic severity.

treatment management procedures.
Treating electrolyte abnormalities Lowering filling pressures

The First Line of Medicine
Systolic failure syndromes - Initiate at low dosages and titrate as tolerated to target doses; either an ACE inhibitor or an ARB is equally efficacious and should be considered in all patients.
- Sacubitril/valsartan (Entresto), a combination medication including a neprilysin inhibitor and valsartan (ARNI), was approved in 2015 as an alternative to an ACE/ARB for the treatment of systolic heart failure (ejection fraction [EF] 40%).
– Morbidity and mortality in patients who have been stable on an ACE or ARB may be further decreased by switching to an ARNI, with careful monitoring required for hypotension and angioedema (all cause mortality reduction around NNT 33 over 2 years of treatment).
Diuretics with loops
May need to be administered initially by IV and later orally if the patient is stabilized.
- 40 to 120 mg/day or TID of furosemide 
A blockers
In cases of abrupt decompensation or poor cardiac output, use with caution.
Start with small doses and increase as tolerated.
- Bisoprolol, 1.25 to 10 mg/day; metoprolol succinate, 12.5 to 200 mg/day; or carvedilol, 3.125 to 25 mg BID (3)
[A] - Aldosterone antagonists, such as spironolactone or eplerenone - Digoxin, 0.125 to 0.250 mg/day for symptomatic patients on conventional therapy for New York Heart Association (NYHA) II to IV heart failure, EF 35% (3)[B]
- For all patients with reduced EF and symptoms that are only partially responsive to ACE inhibitors and beta-blockers, combination hydralazine/isosorbide dinitrate is the first-line treatment for African American patients with classes III and IV symptoms who are already receiving conventional medication.
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Contraindications
Blockers: second- or third-degree heart blocks, reduced cardiac output 
Verapamil and diltiazem should not be used in patients with systolic dysfunction.
Aldosterone antagonists: renal dysfunction, oliguria, and anuria 
Hypokalemia and hypomagnesemia caused by loop diuretics
ACE inhibitors: angioedema and pregnancy
Patients using ACE inhibitors now or within the previous 36 hours, as well as those with a history of angioedema, should take ARNIs. 
Safety measures
Digoxin dose in individuals with chronic kidney disease should be kept to less than 0.125 mg per day, and medication levels should be closely monitored to prevent toxicity.
- Keep an eye on electrolytes.
- ARNIs and ACE inhibitors: Start with caution if blood pressure is low.
Blockers should be avoided in patients who have signs of poor tissue perfusion since they could further impair systolic performance.
- Cilostazol, NSAIDs, and Glitazones are medications to avoid. Milrinone and dobutamine are also drugs to avoid.

Second Line: Continuous inotrope infusion in stage D outpatients for symptom control in those who are ineligible for transplantation or mechanical circulatory support. Inotropic therapy (e.g., dobutamine or milrinone) for cardiogenic shock and support prior to surgery or cardiac transplantation.


A heart failure team's factors for referral management improve results and enable early transplant referral.

Further Treatments
For individuals with a left ventricular ejection fraction (LVEF) 35% and mild to moderate symptoms, a prophylactic implanted cardioverter-defibrillator (ICD) should be taken into consideration.

Patients in sinus rhythm with a QRS >150 ms, LVEF 35%, in functional class (FC) I to III, and ambulatory FC IV patients should be given cardiac resynchronization therapy (CRT) consideration.
Patients with severe, refractory heart failure who have no realistic chance of recovering shouldn't be given the option of getting an ICD. In such cases, palliative care is a viable alternative.
In some stage D patients, it is reasonable to consider an LV assist device as "permanent" or destination therapy or heart transplantation.

Constant Care 
fluid restriction, low-fat, low-sodium diet

Prognosis In NYHA FC IV, 20–40% of patients pass away within a year. One-year survival after a transplant is up to 94%.

Congestive heart failure complications include syncope, renal failure, arrhythmias, or sudden death