Hospital-acquired Acinetobacter baumannii treatment

What does "Acinetobacter baumannii" mean?

Acinetobacter baumannii is a highly drug-resistant bacterium that mostly causes illnesses people get in hospitals, like pneumonia, bloodstream infections, urinary tract infections, and wound infections. The type of cell is a Gram-negative, opportunistic pathogen. It lives in dirt, water, hospital surfaces, ventilators, and catheters. People who are very sick, on ventilators or tubes, or who have open wounds are at a higher risk. Colonisation vs. infection: Some people may carry the bacteria without any signs (colonisation), but it can cause serious infections in weak people.

Acinetobacter Baumannii

Most Common Infections

Get pneumonia in the hospital, especially if you use a respirator.
Sepsis is an illness of the bloodstream.
Urinary tract diseases (catheter-related).
Sores and wounds that need care.
Meningitis, endocarditis, and diseases of the bones and soft tissues happen less often.

Why is it a Major Concern?

Multidrug resistance (MDR): Many strains are not responding to carbapenems, cephalosporins, or aminoglycosides, which means there aren't many treatment options.
Persistence: Can live on hospital surfaces for a long time, which makes breakouts hard to control.
High death rate: invasive infections like sepsis or pneumonia can kill more than 40–60% of severely ill patients.

Diagnosis:

Samples for diagnosis: Blood, urine, mucus from the lungs, and wound swabs.
Tests include Gram stain, culture, biochemical identification, and antibiotic sensitivity testing.

How does Acinetobacter spread?

The main transmission routes

The most common method is through the hands of healthcare workers. Bacteria can spread from one patient to another if proper hand hygiene is not maintained.
Surfaces like bed rails, doorknobs, ventilators, catheters, and medical tools can hold the bacteria for a long time in a hospital setting that is contaminated.
Infected medical tools include ventilators, urinary catheters, and intravenous lines.
Person-to-person contact is less common, but it can happen in healthcare situations where there isn't enough infection control.
The genus Acinetobacter can be found in dirt and water, but A. baumannii infections rarely happen outside of hospitals.

Who is at risk?

Individuals in the ICU who are on ventilators or tubes are susceptible to infection.

Individuals with burns or open wounds are also at risk.
Individuals with weaker immune systems, such as those suffering from cancer, transplants, or diabetes, are also at risk.
Those on broad-spectrum antibiotics, which harm healthy bacteria and facilitate the growth of resistant bacteria, are also at risk.

What's wrong with the transmission

A. baumannii can live on dry surfaces for weeks at a time.
Resistance: Multiple drugs cannot easily kill many strains, making the management of breakouts challenging.
Colonisation vs. infection: People may carry the germs around without getting sick, but they can later give them a very bad illness.

Is Acinetobacter baumannii serious?

Multidrug resistance (MDR): Many types resist carbapenems, cephalosporins, and aminoglycosides, leaving few treatment options.
High death rate: Between 40 and 60% of severely ill patients who get invasive infections like ventilator-associated pneumonia or sepsis die.
Persistence in hospitals: It can live for a long time on surfaces, medical equipment, and even skin, which makes it hard to control breakouts.
Opportunistic: Healthy people don't get infected very often, but people with weak immune systems, open cuts, or medical devices like catheters or ventilators are more likely to get sick.

Types of Infections

Pneumonia (especially when linked to a respirator).
Sepsis is an illness of the bloodstream.
Urinary tract diseases (catheter-related).
Sores and wounds that need care.
Meningitis, brain tumors, and endocarditis are less common but very dangerous.

What Causes Risk

The risk factors include placement in the ICU or prolonged hospital stays.
These risks may include mechanical breathing or the use of catheters that remain in the body for extended periods.
When you have cancer, a donation, or diabetes, your immune system weakens.
You should seek medical advice before using broad-spectrum antibiotics, as they target resistant strains.

Problems with Treatment

There aren't many choices. Colistin, tigecycline, and some newer mixtures of β-lactam and β-lactamase inhibitors are used, but resistance is growing.
Combination therapy: To get better results, doctors sometimes use more than one drug at the same time.
Experimental methods: Antimicrobial peptides and phage treatment are being looked into.

Where did the Acinetobacter baumannii come from?

In hospitals, the germs can live for a long time on surfaces, bed rails, ventilators, catheters, and other medical gear.
Direct contact: It can be passed from healthcare workers' or patients' dirty hands to other people.
They can be found in dirt, water, and sometimes food, but infections that happen outside of hospitals are not common.
Colonization: Some people carry the bacteria on their skin or in their lungs without showing any symptoms. If their immune system is weak, the bacteria can later cause an infection.

Also read https://www.sciencedirect.com/science/article/abs/pii/S2173572722002375

How do people get sick with it?

Patients who use breathing machines are more likely to develop ventilator-associated pneumonia.
Intravenous lines and devices are frequently the source of bloodstream infections.
Infections of the urinary tract: Especially in people who have urinary tubes that stay in their bodies.
Infections in wounds: Burns, surgery wounds, and trauma sites can get infections.

What Causes Risk

Long stays in the hospital or ICU can increase the risk of infection.
Long stays in the hospital or ICU may involve mechanical ventilation or the use of gadgets inside the body.
Cancer, transplants, diabetes, and other serious illnesses can weaken the immune system.
Before using broad-spectrum antibiotics, it is important to select resistant strains.

Prevention

Safety First
Healthcare workers and guests must wash their hands very well.
Cleaning and disinfecting hospital surfaces and tools.
Staff members should wear safety measures such as gloves and gowns during contact.
Use antibiotics wisely to reduce resistance.

Can you get rid of Acinetobacter?

Acinetobacter baumannii infections can be cured, but many strains are resistant to many drugs.

How It's Possible to Get Better

Targeted antibiotics: To find out which drugs work against a certain strain, doctors use culture and susceptibility testing.

Open options:

It is often used for types that are resistant to more than one drug.
Tigecycline—it can help with serious infections sometimes.
Combinations with sulbactam can be helpful in some situations.
There are new drugs on the market, such as cefiderocol or β-lactam/β-lactamase inhibitor combos.
Combining two or more antibiotics improves their effectiveness. This is called combination treatment.
Supportive care: It is essential to remove infectious devices like catheters and ventilators, treat sepsis, and keep the patient stable.

Problems

Multidrug resistance (MDR): Common medicines are ineffective in killing many strains.
How dangerous last-resort drugs are: Colistin, for example, can hurt nerves and kidneys.
High death rate: Even with care, severe infections like ventilator-associated pneumonia or bloodstream infections can still kill.

Treatment for Acinetobacter baumannii

The video on the treatment of Acinetobacter baumannii

Standard Ways of Treating
Testing for culture and sensitivity is the most important part of treatment. Doctors compare the bacteria to medicines that are already on the market to find ones that work.
Agents that are often used:
Colistin, also known as polymyxin E, is often used to treat strains that are immune to multiple drugs, but it can be harmful to nerves and kidneys.
Tigecycline: It can sometimes help with diseases that are hard to treat.
Sulbactam-containing regimens: These are useful when the strain is still vulnerable.
If the strain is still sensitive, carbapenems like imipenem and meropenem should only be used.

Fresh and new choices

Cefiderocol is a new siderophore cephalosporin that appears to be effective against carbapenem-resistant A. baumannii bacteria.
β-lactam/β-lactamase inhibitor mixtures, like sulbactam-durlobactam, are being tested in humans right now.
Antimicrobial peptides and phage treatment are two experimental methods being looked at to treat infections that are resistant to other drugs.

Having trouble with treatment

Multidrug resistance (MDR): Common medicines cannot kill many strains.
Toxicity of last-resort drugs: Colistin works, but it can have severe side effects.
High death rates: Even with care, severe infections like ventilator-associated pneumonia or bloodstream infections can kill.

Helpful and Safeguarding Steps

Device care includes removing or replacing infected catheters, ventilators, or IV lines.
Supportive care includes treating sepsis, giving the patient air and fluids, and keeping them stable.
Strict virus control: hospitals clean their environments, wash their hands, and put people in isolation.
The careful use of antibiotics to slow the growth of resistance is called antibiotic stewardship.

Conclusion

Acinetobacter baumannii is a dangerous hospital-acquired pathogen that is a big problem all over the world because it can live on surfaces, spread in healthcare settings, and not be killed by many antibiotics.

Acinetobacter baumannii infections are curable, but they are difficult to treat due to their resistance to many drugs. Prevention is just as important as treatment. One way to do this is to keep hospitals clean and use antibiotics wisely.

Peripartum Cardiomyopathy safety considerations

Peripartum Cardiomyopathy Safety Considerations

What Is Peripartum Cardiomyopathy (PPCM)?

Peripartum Cardiomyopathy (PPCM) is a rare but deadly form of heart failure that develops in women without cardiac disease in the last month of pregnancy or the first five months following delivery. It can't pump blood well when the heart muscle weakens and enlarges

Key PPCM Features

Cardiomyopathy is specific to pregnancy and postpartum. Cardiomyopathy is typically diagnosed in the final month of pregnancy or five months postpartum. Systolic dysfunction (low ejection fraction, typically <45%) is caused by enlarged heart chambers and muscle weakness. PPCM affects 1 in 2,000 newborns worldwide.

Symptoms

Normal pregnancy changes can mask symptoms, making diagnosis difficult:
Shortness of breath (particularly when lying down)
Reduced exercise tolerance and fatigue
Leg, ankle, or foot swelling
Heart palpitations or fast beat
Cough or chest pain persists

Possible Risks

Conditions that enhance PPCM risk:
Pre-eclampsia, gestational hypertension
Twin or triple pregnancies
Mother's advanced age
Nutritional inadequacies (some places lack selenium)
Genotype
Black women have a higher incidence.

Core insights

Approximately 70% of women recover within one year of diagnosis.
Complications include heart failure, arrhythmias, and thrombosis, as well as mechanical support or transplantation in difficult situations.
Unresolved PPCM increases the likelihood of recurrence and worsened cardiac function in future pregnancies.

Major Postpartum Cardiomyopathy Causes

"No single reason explains all cases, although numerous crucial systems are involved."

1. Vascular and Hormonal Stress

Cleaved prolactin from breastfeeding can harm cardiac muscle cells and blood arteries.
Increased free radicals during pregnancy might cause this damaging cleavage.
Endothelial dysfunction: The blood vessel linings deteriorate, reducing blood flow and injuring the heart muscle.

2. Immune/inflammatory factors

Autoimmune response: A woman's immune system may change during pregnancy, causing cardiac inflammation.
Inflammation of the cardiac muscle can result from viral infections or immunological activation.

3. DNA susceptibility

Some women with PPCM have dilated cardiomyopathy gene mutations.
Risk of cardiomyopathy increases with family history, suggesting genetics.

4. During pregnancy, hemodynamic stress

Pregnancy causes a ~50% increase in blood volume and cardiac output.
This higher workload can reveal cardiac muscle weakening in sensitive women.

5. Nutrition and Environment

In some places, PPCM is linked to selenium and iron deficits.
Geographic variation: Higher frequency in Africa and South Asia reflects environmental or nutritional factors.

Four cardiomyopathy symptoms?

Key Cardiomyopathy Signs

These four symptoms commonly imply cardiomyopathy:

1. Dyspnea (Shortness of Breath)

Dyspnea occurs either during rest or during exercise.
Usually, the condition deteriorates when lying down.
Poor cardiac pumping causes lung fluid accumulation.

2. Fatigue and Weakness

Even after resting, exhausted.
Low exercise tolerance.
This is often caused by inadequate blood flow to the muscles and organs.

3. Edema (swelling)

Edema typically occurs in the ankles, feet, legs, or abdomen.
This condition is typically brought on by fluid retention related to heart failure.

4. Heartbeat irregularities (arrhythmias/palpitations)

The symptoms may include fluttering, hammering, or skipping beats.
Extreme cases may cause dizziness or fainting.

Other Possible Signs

Chest pain or pressure may occur, especially during physical exertion.
Abnormal rhythms cause dizziness or syncope.
Fluid overflow can cause neck vein distension.
The exam revealed heart murmurs.

Why These Signs Matter

Early detection is critical because many of these symptoms match typical pregnancy/postpartum changes or other disorders.
Cardiomyopathy worsens over time if neglected.
Potential complications: Severe arrhythmias, cardiac failure, and thrombosis.

What tests prove cardiomyopathy?

Key Cardiomyopathy Tests

1. Echocardiogram

Most critical test: Ultrasound cardiac imaging.
Displays chamber size, wall thickness, EF, and valve function.
This test confirms the presence of restricted, hypertrophic, or dilated cardiomyopathy.

2. ECG/EKG

Heart activity is recorded.
The ECG/EKG checks for arrhythmias, conduction abnormalities, and hypertrophy.
An initial test is usually requested when symptoms occur.

3. Chest X-ray

This test reveals signs of cardiac hypertrophy and lung fluid accumulation.
It aids in differentiating between cardiomyopathy and lung disease.

4. Blood Tests

BNP: High in heart failure.
Thyroid, renal, liver, and iron tests are conducted to exclude any secondary causes.

5. MRI cardiac

An MRI cardiac scan provides detailed information about the cardiac muscle and scarring.
This scan aids in distinguishing between myocarditis and cardiomyopathy.

6. Pharmacologic or Exercise Stress Test

Assesses cardiac response to exercise.
This test checks for ischemia or exercise-induced arrhythmias.

7. Catheterisation (Angiography)

This procedure is utilised when there is a suspicion of coronary artery disease.
This procedure is used to monitor coronary blood flow and intracardiac pressure.

What organs does cardiomyopathy affect?

Any cardiac muscle condition is a cardiomyopathy. In cardiomyopathy, the heart cannot pump blood well. Sometimes the heartbeat is disrupted.

Which patient is more susceptible to cardiomyopathy?

Some cardiomyopathy risk factors are unchangeable:
A family history of heart failure, cardiomyopathy, or sudden cardiac arrest increases susceptibility.
Personal heart attack history.
The individual has a history of chronic cocaine or alcohol use.
Pregnancy.
The death of a loved one is stressful.

Prevention of cardiomyopathy:

Lifestyle precautions
Nutrition Balanced
Enjoy fruits, veggies, healthy grains, and lean proteins.
Saturated, trans, and added sugars and salt should be limited.
Maintain micronutrient intake (iron, selenium, and magnesium).
Regular exercise
Strive for 150 minutes of moderate exercise every week (walking, cycling, swimming).
If you have cardiac problems, avoid strenuous exercise.
Manage Weight
Maintain a healthy weight to prevent cardiac strain.
Cardiomyopathy can result from obesity-related hypertension and diabetes.

Medication Warnings

Manage Hypertension, Diabetes
Uncontrolled diabetes and high blood pressure destroy the heart muscle.
Regular monitoring and drug compliance are essential.
Check Cholesterol.
Cardiomyopathy worsens with high cholesterol and coronary artery disease.
Regular Checkups
If you have a family history of cardiomyopathy, an ECG may be recommended.
Treatment and lifestyle changes are possible with early detection.

Stay away from harmful substances

Stop smoking: Tobacco damages blood arteries and increases heart disease.
Limit Alcohol: Alcohol weakens the heart muscle (alcoholic cardiomyopathy).
Stop using illegal drugs: Cocaine and amphetamines damage the heart.

Risk Awareness

Family history: Cardiomyopathy is best treated with genetic counseling and early screening.
Peripartum cardiomyopathy (PPCM) should be examined, especially in women with hypertension or numerous pregnancies.
Viral myocarditis and autoimmune disorders can lead to cardiomyopathy; therefore, it is important to seek medical attention if you experience unexplained fevers or chest pain.

Its treatment?

The video about the Story of Survival and Recovery

Cardiomyopathy is treated with drugs, lifestyle changes, and, in difficult situations, surgery or medical devices. We aim to improve heart function, alleviate symptoms, and prevent heart failure and arrhythmias.

1. Medications

Beta-blockers: Lower heart rate and boost pumping.
ACE/ARB inhibitors lower blood pressure and cardiac strain.
Diuretics reduce edema and dyspnea by removing excess fluid.
Anticoagulants: Used to prevent blood clots in patients with significant cardiac hypertrophy or arrhythmia.
Control irregular heartbeats with antiarrhythmics.
ARNIs: Newer heart failure medications that improve outcomes.

2. Lifestyle changes

A low-salt, heart-healthy diet that includes fruits, vegetables, and lean proteins is recommended.
Avoid overexertion and exercise moderately.
Stop drinking and smoking: They destroy the heart muscle.
Weight control: Reduces heart strain.
Reduce cardiovascular stress using yoga, meditation, or counseling.

3. Medical Gear

ICD: Corrects harmful arrhythmias to prevent abrupt cardiac death.
A pacemaker regulates slow or irregular heartbeats.
CRT coordinates contractions in heart failure and conduction abnormality patients.

4. Surgery Choices

Septal myectomy: Removes thickened heart muscle for hypertrophic cardiomyopathy.
In end-stage cardiomyopathy, a heart transplant is considered when other therapies fail.
LVAD: A mechanical pump that sustains heart function in difficult situations.

5. Monitoring, Follow-up

Regular echocardiograms monitor heart function.
Blood tests (BNP, electrolytes) are performed to track the progression of heart failure.
Holter arrhythmia monitoring.
Family history-related genetic counseling.

Conclusion

Cardiomyopathy is a dangerous but treatable condition that impairs the heart's ability to pump blood. Genetics, pregnancy-related stress (peripartum cardiomyopathy), lifestyle, or secondary medical disorders might cause it. Cardiomyopathy is not always preventable, although prompt medical attention and follow-up significantly improve results. Understanding signs, causes, and treatments empowers patients and caregivers to improve heart health.

Vestibular Neuritis rehabilitation with a physical therapist

Vestibular Neuritis (Vestibulopathy)—Info:

Vestibular neuritis is caused by inflammation of the vestibular nerve, leading to sudden, severe vertigo, dizziness, balance problems, nausea, and vomiting. Viruses are usually to blame for this condition, which affects the brain's spatial orientation nerve.

Exactly What Is Vestibular Neuritis?

Vestibular neuritis is an inflammation of the vestibular branch of the vestibulocochlear nerve (cranial nerve VIII), which sends balance signals from the inner ear to the brain. Balance and spatial orientation signals are disrupted, creating vertigo and instability. Labyrinthitis affects both balance and hearing, whereas vestibular neuritis only affects balance.

Symptoms

Instant, acute vertigo lasting hours to days
Dizziness and unsteadiness
Disrupted balance signals cause nausea and vomiting.
Involuntarily moving eyes
Contrary to labyrinthitis, there is no loss of hearing.

Causes

Most triggers are viral diseases such as colds, flu, and herpes.
Rarely, bacterial infections or autoimmune reactions may cause it.
Inflammation of the vestibular nerve disrupts brain signalling.

Diagnosis

Clinical evaluation: Neurological and balance testing.
Rule out stroke, Ménière's disease, or multiple sclerosis.
Imaging (MRI/CT): Used to rule out CNS causes.

Treatment

The video about vestibular therapy

Manage symptoms with short-term usage of vestibular suppressants.
Anti-nausea drugs
Corticosteroids: Reduce nerve inflammation for some.
Brain retraining and balance exercises are a vestibular rehabilitation treatment (VRT).
Most patients recover within a few weeks, though mild imbalances can last months.

Important Info

An acute episode of vestibular neuritis can be severely debilitating but not fatal.
Rest, rehabilitation, and time typically fix it.
Hearing is preserved, unlike labyrinthitis.
Early medical evaluation helps rule out stroke.

Vestibular neuritis—brain damage?

Vestibular neuritis is not a brain injury. It is an inner ear condition caused by vestibular nerve inflammation that impairs brain-sent balancing signals. Though severe and disabling, vertigo and dizziness do not damage the brain.

Important Difference

The difference lies in the inflammation of the inner ear vestibular nerve.
Damage to brain tissue can occur due to stroke, trauma, or neurodegenerative illness.
Difference: Vestibular neuritis affects brain signal input, not brain tissue.

Causes of Symptom Confusion

The vestibular nerve links the brainstem and inner ear.
During inflammation, the brain misinterprets balance information due to incorrect or decreased impulses.
This produces vertigo, imbalance, nausea, and nystagmus, which resemble neurological issues.
Unlike stroke or brain injury, hearing and brain tissue frequently survive.

Recovery, Outlook

Extreme vertigo can persist for hours to days.
Most people recover within weeks as the brain adapts (central compensation).
Long-term: Some have a lasting imbalance but no brain damage.
Treatment options include anti-nausea and vestibular suppressants, steroids, and vestibular rehabilitation.

Important info

Vestibular neuritis is inner ear nerve irritation, not brain injury.
Though strong, symptoms are usually transient.
Vertigo can overlap with neurological problems; thus, medical evaluation is necessary to rule out stroke or other brain conditions.
Most patients recover totally with proper care.

Recovery from vestibular neuritis

Depending on severity and individual conditions, vestibular neuritis might take 4–6 weeks to 2–3 months to fully recover. Most people recover within a few weeks. Patients may have months-long imbalances.

Typical Recovery Time

First few days: Acute phase

The acute phase is characterised by sudden, acute vertigo, nausea, vomiting, and instability.
This stage has the most severe symptoms.

Subacute phase (1–4 weeks): Vertigo progressively improves.

When moving fast or in visually complex situations, patients may feel shaky.
During the recovery phase (4–8 weeks), many patients achieve a near-normal balance.
Central compensation helps the brain use signals from the unaffected ear.
Extended recuperation (2-3 months) may cause minor dizziness or imbalance in certain individuals.
Stress, fatigue, and illness can increase symptoms.

Recovery Factors

Age: Recovery may be slower for seniors.
Nerve irritation severity: Severe instances slow healing.
Early treatment: Corticosteroids and VRT enhance recovery.
Lifestyle: Exercise and balancing activities speed brain adaptation.

Managing Recovery

Vestibular suppressants and anti-nausea medications are used for acute symptoms.
Balance and dizziness exercises are part of vestibular rehabilitation therapy (VRT).
Walking and other gentle activities speed up compensation.
Avoid overrest: Bed rest slows healing.

Key points

Most recover in 4–8 weeks, although full recovery may take 3 months.
Some imbalances last for months.
Faster and more complete healing requires vestibular rehabilitation.
A medical assessment is necessary to rule out stroke and other potential causes of vertigo.

Exercises for VN

Vestibular rehabilitation treatment (VRT) involves vestibular neuritis exercises that retrain your brain to respond to balance signals and reduce dizziness. Gaze stabilisation, balance training, and habituation exercises are most effective when performed daily for 20–30 minutes.

Main Exercise Types

1. VOR Training: Gaze Stabilisation

Improve head-moving eye control.
Sit or stand and gaze on a stationary object (such as a wall letter).
Raise or lower your head while keeping your eyes fixed.
Start slowly, then accelerate as tolerated.
Benefit: Reduces head-movement blurring and dizziness.

2. Balance Exercises

Increase stability and postural control.
Stand with feet together, then one foot.
Walk straight, heel-to-toe.
Experiment with head-turning while walking.
Keep yourself safe by performing near a wall or with assistance.

3. Practice Habituation

Repeating symptom-causing movements reduces dizziness.
Sit, rapidly lie down, and sit up (perform multiple times).
Sit or stand with your head turned.
Bend forward to grab something, then stand.
Expect little dizziness to help the brain adapt.

4. Functions

Daily walks: Even small ones improve balance.
Walk with your head turned left/right.
Walking while counting or carrying an object tests coordination.

The frequency and duration

The frequency and duration should be two to three 20–30-minute sessions per day.
Progress: Start with simple movements, then add speed and complexity.
Recovery requires consistency: daily practice.

Safety Tips

Mild dizziness is normal during adaptation.
Don't overdo it: Exercise should challenge but not fatigue.
Environment: Start in a safe place with someone nearby.
For stability during standing activities, wear flat shoes or go barefoot.

Whom should I see for vestibular neuritis?

Vestibular neuritis specialists differ based on the stage of symptoms and the need for diagnosis or rehabilitation.

Consult Specialists

ENT Specialist (Otolaryngologist): Initial contact.

Examines inner ear problems, ruling out labyrinthitis, Ménière's, and infections.
The ENT specialist prescribes anti-nausea, vestibular suppressants, and corticosteroids.

Neurologist

Consult a neurologist for severe or abnormal symptoms or to rule out stroke/neurological reasons.
After conducting thorough neurological evaluations, the neurologist may order MRI/CT scans.

Audiologist:

The audiologist evaluates the function of hearing and balance.
Labyrinthitis (hearing loss) may overlap, making this important.

Balance-specialised physical therapist:

A balance-specialised physical therapist assists patients with vestibular rehabilitation.
The treatment plan encompasses techniques such as gaze stabilization, balancing, and habituation exercises.
This is crucial for promoting long-term healing and reducing symptoms of dizziness.

When to Get Help Now

For sudden vertigo, weakness, slurred speech, double vision, or severe headache, seek emergency examination to rule out stroke.
For persistent vomiting or inability to walk safely, seek medical attention immediately.

Conclusion

An inner ear illness called vestibular neuritis causes sudden vertigo, dizziness, and balance issues due to vestibular nerve irritation. Disrupted inner ear balancing signals are the issue, not brain damage. Some people may have an imbalance for months after 4–8 weeks of recovery. Gaze stabilisation, balance training, and habituation techniques can speed up recovery and help the brain adapt. Medical evaluation is needed to rule out stroke; most patients recover with careful care.

How to get rid of dermatillomania

How to get rid of dermatillomania?

Dermatillomania—Overview

Dermatillomania, also known as excoriation disorder or skinpicking disorder, is characterized by compulsive picking at one's skin, which causes tissue damage, infections, and scarring. It belongs to the OCD spectrum. Psychotic Dermatillomania (Excoriation Disorder) causes bodily injury. DSM-5 classifies it as Obsessive–Compulsive and Related Disorders.

Symptoms

Excessive picking of the skin, scabs, acne, or perceived flaws.
Sores, bleeding, scars, infections.
Distress: guilt, humiliation, anxiety, or low quality of life.

Causes

Multifactorial causes: Genetic predisposition.
Mental issues such as OCD, stress, and anxiety also play a significant role.
Environmental factors such as boredom, stress, and sensory cravings also play a significant role.

Impact

Physical health risks: infections, delayed wound healing, permanent scars.
This can lead to heightened feelings of anxiety, despair, and social isolation.

Options for Management and Treatment

CBT: Especially Habit Reversal Training (HRT), which helps people identify triggers and replace picking with better habits.
In difficult situations, SSRIs and other psychiatric drugs may be administered.
Lifestyle tips: Trim nails.
Consider using stress balls or fidgets.
Bandaging afflicted areas.
Relaxation and mindfulness.

Risks and Factors

Delayed diagnosis: Embarrassment causes many to hide symptoms, exacerbating damage.
It frequently co-occurs with OCD, anxiety, and depression.
Need for expert help: Self-management typically requires psychiatric or psychological support.

What therapist treats dermatillomania?

Skin-picking disorder, dermatillomania, is best treated by clinical psychologists or psychiatrists who specialize in OCD and similar disorders. CBT, particularly HRT, is the best method. Dermatologists may treat skin damage, although psychologists and psychiatrists are usually the main therapists.

Therapist Types: Those who treat dermatomania

1. Clinical psychologists

CBT and HRT psychotherapy are recommended.
Help patients recognise triggers, learn coping skills, and adopt better picking habits.
Relapse prevention and long-term behaviour change.

2. Psychiatrists

Medical mental health specialists.
Recognise excoriation disorder, administer SSRIs and N-acetylcysteine, and coordinate care.
They are recommended for treating severe depression, anxiety, and OCD.

3. Dermatologists

Treat skin-picking injuries, infections, and scars.
Give wound care, topical therapies, and cosmetic recommendations.
Best for: Skin care and psychotherapy.

4. Specialised BFRB Therapists

BFRB therapists treat trichotillomania and dermatillomania.
Focus: Customized CBT, mindfulness, and acceptance therapies.
Ideal for: Specialised patients.

Important Considerations

Psychologists, psychiatrists, and dermatologists work best together for therapy, medicine, and skin health.
Early intervention reduces scarring and psychological anguish.
Online therapy: BetterHelp and PsychologyHelp match patients with dermatillomania-trained therapists.

How prevalent is dermatillomania?

Dermatillomania (excoriation condition) affects 1.4%–5.4% of the population, more than many realize. Shame and embarrassment lead individuals to conceal their symptoms, resulting in underdiagnosis of the condition.

Epidemiology and prevalence

1.4%–5.4% of individuals develop dermatillomania, according to studies.
Gender differences: Women are more affected, although men are too.
It usually starts in youth or early adulthood, around the time acne or skin changes are widespread.
Underreporting: Many cases are overlooked because people perceive it as a “bad habit” rather than a mental illness.

Why It's Missed

Patients may avoid care owing to stigma and guilt regarding visible scars or wounds.
Overlap with other disorders: OCD, anxiety, sadness, and body dysmorphic disorder sometimes disguise its presence.
Mental illness is sometimes misdiagnosed as dermatological.

Co-occurrence with other conditions

OCD is compulsive.
Body-centered repetitive behaviors (BFRBs) include trichotillomania.
Depression and anxiety: High comorbidity increases disease burden.

Can dermatillomania be cured?

Dermatillomania (excoriation disorder) is a chronic mental illness whose "cure" is rarely mentioned. Instead, professionals discuss management, treatment, and rehabilitation. With the correct therapy, medicine, and lifestyle changes, many patients improve and even go into remission.

Treatment Prospects

Why “cure” is challenging

Dermatillomania, like OCD and trichotillomania, is a body-focused repetitive activity.
Symptoms fluctuate with stress, surroundings, and mood.
Relapses are possible; therapy can greatly reduce severity and frequency.

Treatments Based on Evidence

1. Psychotherapy

CBT helps discover triggers and change mental habits.
Habit Reversal Training (HRT): Addresses impulses and promotes healthy habits.
ACT decreases compulsive plucking and builds discomfort tolerance.

2. Drug

Some SSRIs lessen compulsive cravings.
Some research has demonstrated that N-acetylcysteine (NAC) reduces BFRB symptoms.
Medication is generally used with therapy.

3. Dermacare

Wounds, scars, and infections become less embarrassing and painful when treated.
Bandages and barrier creams minimize picking.

4. Manage Yourself

Keep nails short.
Use stress balls or fidget toys.
Practice mindfulness and reduce stress.
Cover sensitive areas with clothing or bandages.

Test for skin picking

To better understand your symptoms, take a free online self-assessment exam for dermatillomania (skin-picking disorder). These tests are screening tools and do not replace a professional diagnosis.

Recommended Online Skin-Picking Disorder Tests

1. SkinPick.com Dermatillomania Test

The test utilizes a validated scale-based questionnaire, such as the Skin Picking Scale-Revised and Milwaukee Inventory.
The test identifies the symptoms and severity of excoriation disorder.
Review your 7-day behavior.
Available from SkinPick.com

2. Online Dermatillomania Quiz

Complete clinical self-assessment.
Skin-picking frequency, intensity, and effects are assessed.
This information should only serve as a guide.
It is not a substitute for seeking medical advice.
Online Dermatillomania Test Toolkit

3. Dermatillomania OCD Screening MantraCare

The survey is simple and provides immediate results.
Screens for compulsive skin-picking and its effects on daily life.
Connects therapists if needed.
MantraCare OCD Dermatillomania Test

These tests measure

The MantraCare OCD Dermatillomania Test measures the frequency of picking (never, rarely, sometimes, often, or always).
The tests distinguish between minor scratches and the level of harm caused by wounds or scars.
Ineffective attempts to stop.
The condition can cause distress, embarrassment, and disruption to daily life.

Vital Considerations

Autotests aren't diagnostic. It is important to determine whether your symptoms are indicative of dermatillomania.
Professional assessment is crucial. A psychologist or psychiatrist can diagnose and treat.
Early intervention is important. Assistance can prevent scarring, infections, and emotional distress.

Dermatillomania therapy

The video is about tips to avoid skin picking.

Skin-picking condition can be treated with psychotherapy, medicine, and dermatology. The most successful treatment is Cognitive Behavioral Therapy (CBT) with Habit Reversal Training (HRT), often combined with SSRIs or N-acetylcysteine, wound care, and lifestyle changes.

Main Treatment Methods

1. First-line psychotherapy

CBT helps patients discover triggers and change cognitive patterns.
Habit Reversal Training (HRT): Addresses impulses and promotes healthy habits.
ACT decreases compulsive plucking and builds discomfort tolerance.
Body-focused repetitive behaviours such as trichotillomania and dermatillomania necessitate specialized BFRB treatment.

2. Adjunctive medication

Reduce anxiety and obsessive cravings with SSRIs.
N-acetylcysteine (NAC), an amino acid supplement, reduces compulsive picking in studies.
Sometimes antipsychotics or glutamatergic medications are used in resistant patients.
3. Dermacare
Initial treatment: wound care, antiseptics, and infection surveillance.
Permanent skin repair: Hydroquinone for pigmentation, silicone for scars.
Prevention: Bandages, barrier creams, and safety gear.

Risks and Factors

Stress might trigger relapse; therapy helps maintain remission.
Side effects of SSRIs include nausea, sleep disturbances, and sexual dysfunction.
Patients delay therapy owing to embarrassment; education and support groups lessen isolation.
Mental illness is often misdiagnosed as dermatological.

Also, read https://www.medicoverhospitals.in/diseases/skin-picking-disorder/.

A Key Note

Although treatable, dermatillomania is rarely “curable.”
A psychologist for treatment, a psychiatrist for medicine, and a dermatologist for skin care get the best results.
Early intervention reduces scarring and psychological anguish.

Conclusion

Dermatillomania, or excoriation disorder, is a mental illness that causes excessive skin-picking and physical and emotional suffering. Though commonly mistaken for a "bad habit," it is part of the body-focused repetitive behaviours (BFRBs) continuum, strongly connected to OCD and trichotillomania. Dermatillomania is serious, curable, and common. Early detection, destigmatization, and multidisciplinary care are crucial for rehabilitation. Patients should know they have support and effective treatment.

Actinic keratosis is most effectively treated

Actinic keratosis—Overview

Actinic keratosis (AK), also called solar keratosis, is a precancerous skin condition caused by prolonged sun exposure. Untreated, rough, scaly patches on sun-exposed areas such as the face, head, ears, lips, forearms, and hands can develop into squamous cell carcinoma. The patches may appear pink, crimson, brown, or flesh-colored. Due to sun exposure, it usually develops in individuals over 40. AK is not contagious.

Actinic keratosis face, head

Possible Risks

Possible risks include outdoor work, tanning beds, and chronic sun exposure.
Light hair, eyes, and skin minimise melanin protection.
Over 40.
HIV and organ transplant recipients are immunosuppressed.

Location:

This condition is more common in sunny climates, such as in South Indian states like Tamil Nadu, where UV exposure is intense.

Possible Issues

If left untreated, 5–10% of AKs develop Squamous Cell Carcinoma (SCC)
Cosmetic issues: Face/scalp patches might impact appearance.
Field cancerization: Multiple AKs imply broad solar exposure.

Diagnosis

Clinical exam: Dermatologists examine patients visually and tactilely.
If the lesion suggests invasive cancer, biopsy.

Ways to prevent

For sun protection, use broad-spectrum sunscreen (SPF ≥30), protective clothes, and helmets.
Stay away from tanning beds.
Patients with AK who are at high risk or have multiple cases should have regular skin checks.
Early treatment can prevent skin cancer.

What causes actinic keratosis?

Main Actinic Keratosis Causes

Long-term UV exposure

Sunlight: The main reason. UV radiation damages keratinocyte DNA through the skin.
Tanning beds and lights emit UV.

Long-term damage

The cumulative effects of daily outdoor activities mount up over decades.
Years of exposure cause lesions, not one sunburn.

Increased Susceptibility Risks

Fair skin, light hair, and light eyes have less melanin.
Over-40s are the most common.
They typically reside in bright or high-UV areas such as South India and Australia.
Job: Outdoor workers (farmers, builders, fishers).
Chronic immunosuppression: Organ transplant recipients or immunosuppressive medication users.
UV exposure causes DNA mutations in skin cells.
Damaged epidermal cells provide rough, scaly areas.
Untreated lesions can become squamous cell cancer.

Can actinic keratosis become cancerous?

AK is a precancerous lesion that, in some cases, can progress to cancer.

Cancer Progression Risk

AKs can lead to Squamous Cell Carcinoma (SCC), a prevalent skin disease.
Studies predict that 5–10% of untreated AKs may develop SCC.
Multiple AKs (field cancerization), lip lesions (actinic cheilitis), or immunosuppression (transplant patients) increase risk.

BCC/Melanoma:

Although AKs don't cause these malignancies, their existence indicates significant UV damage, which raises skin cancer risk.

Malignant Transformation Warning Signs

A thicker, sensitive, or painful lesion is a warning sign of malignant transformation.
Rapid expansion or ulceration.
Unhealing bleeding or crusting.
The condition is compared to the firmness of the adjacent skin.

Monitoring & Prevention

Early AK therapy greatly decreases cancer risk.
If you have several lesions, see a dermatologist regularly.
Protection from the sun (SPF ≥30, hats, clothing) is the best strategy to avoid new AKs and lower progression risk.

Also, read https://dermnetnz.org/topics/actinic-keratosis.

Who is most at risk for actinic keratosis?

High-risk Actinic Keratosis groups

1. Genetics, Skin Type

Fair complexion, light hair, and light eyes result in reduced UV protection due to melanin.
Skin cancer risk increases with family history and genetic predisposition.

2. Age

Risk increases with accumulated sun exposure for individuals over 40.
AKs are rare in youngsters but widespread in middle-aged and elderly individuals.

3. Solar exposure

Outdoor workers such as farmers, builders, fishers, and athletes are susceptible to solar exposure.
Solar exposure also affects people who live in bright climates or near the equator, such as in South India or Australia.
People may have a history of sunburn or exposure to tanning beds.

4. Immune State

Individuals who are on immunosuppressants following an organ transplant are a prime example.
HIV-positive or immunocompromised people.
Reduced immune surveillance lets aberrant cells proliferate unrestrained.

5. Other Risks

Men are more harmed owing to outdoor work and less sunscreen application.
Bald or thinning hair: Increases UV exposure.
Unprotected sunbathing, gardening, sports, and leisure activities increase UV exposure.

Common Actinic Keratosis Symptoms • Texture:

The affected areas may be rough, dry, or scaly, exhibiting a harsh texture. • These regions may exhibit a crusty texture or feature a prominent bulge resembling horns. • Color: red, pink, tan, brown, silvery, or skin-colored. • The color can manifest as discoloured patches or blend in with the surrounding skin. • Size: • The size can vary from a small spot to a diameter of 1 inch (2.5 cm). • Shape and Surface: • Flat or slightly elevated. • Over time, the surface may harden and develop a wart-like appearance. • Location: • Chronic sun exposure areas: face, scalp, ears, lips, neck, shoulders, forearms, and backs of hands. • Progress: • Lesions develop gradually over months to years. • Progressing squamous cell carcinoma may cause thickening, tenderness, or bleeding.

Warning Signs of Medical Concern ·

The tumour may grow quickly or undergo a rapid size shift. • Pain, soreness, or itching. • Ongoing bleeding or ulceration. • The skin appears firmer in comparison to the surrounding skin.

Is the actinic keratosis resolved?

Untreated actinic keratosis (AK) often persists, recurs, or worsens.

Natural Actinic Keratosis Course
Persistence: AK lesions typically stay on the skin without treatment.
Spontaneous Regression: AKs may temporarily fade or disappear when sun exposure is minimised.
The sun damage keeps them from disappearing, so they regularly return.
Untreated AKs can progress to squamous cell carcinoma (SCC) at a rate of 5-10%.
No one can anticipate which lesions will become malignant.

Reasons to Treat

Dermatologists proactively treat precancerous AKs.
Removing them minimises SCC risk and enhances attractiveness.
Cold therapy, topical creams (5-FU, imiquimod, and diclofenac), photodynamic therapy, and laser therapy are used.

Long-term care and prevention

Provide consistent sun protection (SPF ≥30, caps, clothes).
Check skin for new lesions regularly.
Lifestyle changes: Stop using tanning beds and limit noon sun.

How to treat toddler keratosis?

Bathe warmly, not hotly. Use a gentle, soap-free body and face wash. Apply a light moisturizer multiple times a day.

Treating actinic keratosis

The Main Treatments

1. Freezing therapy

Liquid nitrogen is used to freeze and destroy abnormal cells.
Ideal for: Few lesions.
Quick, effective, and low-downtime.
Cons: Possible redness, blistering, or hypopigmentation.
Recurrence: 24% within 12 months if sun exposure continues.

2. Topically applied drugs

5-Fluorouracil (5-FU) cream destroys aberrant cells.
Imiquimod: Boosts the immune system attack on damaged cells.
Diclofenac gel: Milder, slower anti-inflammatory.
Ingenol mebutate: Fast but rarely used.
Best for: Multiple lesions or “field cancerization” (widespread UV damage).
Cons: Treatment may cause redness, inflammation, and peeling.

3. Photodynamic Therapy

A light-activated medication is applied to skin and exposed to specific light.
This treatment is specifically designed for larger areas that have multiple AKs.
Pros: Cosmetically effective, cures visible and unseen lesions.
Cons: Clinic visits, transient pain/redness.

4. Surgery Choices

Curettage and electrocautery: Lesion removal.
Abnormal cells vaporise under laser therapy.
This treatment is particularly effective for thick, resistant lesions.

5. Self-Care, Prevention

Use sunscreen (SPF ≥30) daily on exposed skin.
Protective gear, caps, and sunglasses.
Avoid tanning beds and the noon sun.
Regular dermatology exams should be conducted at least annually following therapy.

Brief Summary

Precancerous actinic keratosis demands active treatment. The most common first-line treatment is cryotherapy, whereas topical creams and photodynamic therapy treat extensive lesions. Sun protection is crucial to preventing recurrence.

Conclusion

Long-term sun exposure causes actinic keratosis (AK), a common precancerous skin disease. Sun-exposed areas develop rough, scaly patches that indicate skin injury. AKs can develop squamous cell carcinoma, so early identification and treatment are crucial.

Prevent, treat, and control actinic keratosis. Consistent sun protection and early medical care work best. AKs are a symptom of cumulative sun exposure, so patients may protect their skin and lower cancer risk.

Kaposi sarcoma cancer treatment guidelines

Kaposi's Sarcoma—Overview:

Kaposi's Sarcoma (KS), a rare malignancy caused by Human Herpesvirus 8 (HHV-8), usually appears as purple, red, or brown skin lesions but can also infect the lungs and gastrointestinal tract. Kaposi's Sarcoma is a type of cancer that affects the lining of blood and lymph vessels. It is strongly connected to reduced immunity, notably in HIV/AIDS and immunosuppressive therapy patients. HIV/AIDS (KS). Patients are often prescribed immunosuppressants following an organ transplant. Elderly males from the Mediterranean/Eastern Europe typically have HIV/AIDS (KS), while sub-Saharan Africans have endemic KS.

Kaposi sarcoma

Symptoms

Skin lesions: Painless purple, red, or brown spots, plaques, or nodules.
Mucosal lesions may appear on the mouth, nose, or anus.
Internal Involvement: Lung or digestive system lesions can cause respiratory problems, bloody coughs, and GI bleeding.

What causes Kaposi sarcoma?

Kaposi sarcoma (KS) is caused by infection with the Human Herpesvirus 8 (HHV-8, also known as KSHV), but not everyone infected with HHV-8 develops KS. The virus needs cofactors like immune suppression to transform cells into cancerous ones, affecting the skin, lymph nodes, and internal organs.

What are the four Kaposi sarcoma types?

Four forms of Kaposi's Sarcoma (KS) are associated with various populations and risk factors:
Traditional KS: Slow, skin-focused older males.
Aggressive African KS can affect children.
Epidemic KS: HIV/AIDS-related, widespread, and expanding.
Often reversible, immunosuppressive therapy causes KS.

How does Kaposi sarcoma spread?

Kaposi's Sarcoma (KS) spreads differently depending on the type and the patient's immunological condition. A breakdown:

Key spread factors

Low immunity (HIV/AIDS, immunosuppressive therapy) promotes spread.
Effective HIV antiretroviral therapy (ART) can stop or reverse KS development.
Internal organ involvement indicates a more aggressive illness; skin-only KS is slower.
Compared to younger, immunocompromised patients, older classic KS patients progress more slowly.

Classic KS: Slow, indolent.

AIDS-related KS: Rapid, life-threatening.
Adjustments to immunosuppressive therapy cause KS.
Kaposi's Sarcoma can range from indolent (developing over years) to aggressive (expanding within months), with HIV-related KS spreading fastest.

Also, read https://emedicine.medscape.com/article/279734-treatment?form=fpf.

Can Kaposi sarcoma be prevented?

Kaposi's Sarcoma (KS) is connected to Human Herpesvirus 8 (HHV-8); however, the best prevention methods focus on immune system health, specifically HIV control and immunosuppressive medication use.

Important Prevention Methods

1) HIV/AIDS Management

The most effective strategy to avoid epidemic (AIDS-related) KS is consistent ART use. ART improves immunity and greatly reduces KS risk.
HIV testing and early treatment: Early HIV detection and ART reduce KS risk.

2. Immunosuppression reduction

If KS develops, transplant doctors may alter or reduce immunosuppressive medicines.
Use immunosuppressive drugs under physician supervision to avoid unnecessary long-term use.

3. General Immune Health

Healthy lifestyle: Balanced food, exercise, sleep, and stress management boost immunity.
Avoiding co-infections like tuberculosis and hepatitis reduces immune strain.

4. Know HHV-8

Transmission: Saliva, sexual contact, and potentially blood spread HHV-8.
Safe practices: Protecting sexual activity and not sharing toothbrushes or razors can reduce risk.
Geographic risk: HHV-8 is more prevalent in sub-Saharan Africa and the Mediterranean; awareness is crucial.

Controllable Risks

Untreated HIV infection represents the highest risk for KS.
Long-term immunosuppression increases risk.
Weakened immunity from poor health or co-infections promotes KS development.

Who has the highest sarcoma risk?

Certain genetic disorders, past radiation therapy, chemical exposure, chronic lymphedema, and weakened immune systems increase sarcoma risk. Sarcoma risk is not highly connected to diet or smoking.

Major Sarcoma Risk Groups

1. Genes and heredity

TP53 mutations cause Li-Fraumeni syndrome.
Familial retinoblastoma (RB1 mutations)
Type 1 neurofibromatosis
Werner syndrome (early ageing)
These disorders enhance bone and soft tissue sarcoma risk.

2. Radiation/chemotherapy history

Radiation for other malignancies can increase sarcoma risk years later.
Secondary sarcomas are linked to alkylating chemotherapy medications.

3. Chemical Encounters

Vinyl chloride, dioxins, arsenic, and pesticides increase sarcoma risk.
In chemical industries, occupational exposure is a risk.

4. Chronic Lymphedema

Chronic limb swelling following breast cancer surgery or radiation can lead to lymphangiosarcoma, a rare sarcoma subtype.

5. Immunosuppression

Individuals who are taking immunosuppressants following an organ transplant are also at risk.
HIV/AIDS patients, particularly those suffering from Kaposi's Sarcoma, also face this risk.

Disconnected Groups

Lifestyle factors such as smoking, eating, and exercising do not increase the risk of developing sarcoma.
Sarcoma is not caused by trauma, but tumors may appear after an injury.

Practical Tip

People with genetic cancer syndromes, radiation/chemo, chemical exposure, chronic lymphedema, or immunological suppression are most at risk.
General population: Sarcoma is infrequent and usually risk-free.

How is sarcoma diagnosed?

Stepwise clinical evaluation, imaging, and biopsy are needed to diagnose sarcoma. Sarcomas are rare and can look like benign masses; thorough diagnosis is necessary.

Common Diagnostic Steps

1 Clinical Exam

Patients describe lumps, swelling, discomfort, or inexplicable symptoms.
Physical exam: Doctors evaluate mass size, position, depth, and growth rate.
Rapidly developing, deep-seated, or painful masses are suspicious.

2. Imaging Studies

MRI is the preferred method for diagnosing soft tissue sarcomas, as it provides information on the size, depth, and proximity to adjacent tissues.
CT scan: Used for lung metastases and bone sarcomas.
Ewing's and osteosarcomas benefit from X-rays.
PET Scan: Used to assess spread or therapy response.

3. Biopsy (final diagnosis)

Core needle biopsy: Preferred; minimally invasive but delivers pathologic tissue.
If needle biopsy fails, incisional biopsy is used.
Excisional biopsy: For tiny, readily removed lesions.
Pathology: Cell morphology and markers confirm sarcoma.

4. Laboratory/Molecular Tests

Immunohistochemistry classifies sarcoma subtypes using particular proteins.
Genetic testing: Finds Ewing's sarcoma's EWS-FLI1 chromosomal translocation.
Although not diagnostic, blood testing can assist measure health before therapy.

5. Staging

Upon diagnosis, clinicians stage sarcoma using:
Tumor depth and size
Spread to lymph nodes or distant organs (lungs)
Depends on how aggressive the cells are histologically

Treatment Choices

The video about causes and treatment for Kaposi sarcoma

Antiretroviral Therapy (ART): First-line HIV-related KS treatment; immune function recovery decreases lesions.
Local treatments: Surgery, cryotherapy, or radiation for lesions.
Systemic therapy: Liposomal doxorubicin, interferon-alpha, or immunotherapy for disease dissemination.
Manage bleeding and respiratory issues with supportive care.

The prognosis varies depending on the immunological status and the severity of the disease.

ART helps HIV-related KS; relapse is probable.
Classic KS: Slow-growing and controllable.
Endemic KS: Aggressive, especially in kids.

Conclusion

Sarcomas are rare, diverse malignancies that affect connective tissues such as bone, muscle, fat, and blood vessels. Kaposi's Sarcoma (KS) is distinct since it is caused by HHV-8 and is connected to immunological suppression.

Kaposi's Sarcoma demonstrates the importance of the immune system in cancer development. Stimulating immunity by HIV therapy, medical management, or a healthy lifestyle is key to prevention and control. Early detection and customized therapy improve outcomes.

Facts about postural orthostatic tachycardia syndrome

Facts about Postural Orthostatic Tachycardia Syndrome

POTS—Overview.

Postural Orthostatic Tachycardia Syndrome is a chronic autonomic nervous system condition that causes an abnormal increase in heart rate (≥30 bpm in adults, ≥40 bpm in adolescents) within 10 minutes of standing, without a significant reduction in blood pressure. It is becoming more common worldwide. Orthostatic intolerance is distinguished by increased heart rate, dizziness, fatigue, and palpitations when standing. The condition is characterized by a dysfunction in the autonomic control of blood flow and heart rate.

Criteria for diagnosis:

Within 10 minutes of standing or tilt-table testing, the heart rate increases by at least 30 bpm in adults and 40 bpm in adolescents.
There is no orthostatic hypotension (a decrease in systolic or diastolic blood pressure of ≥20 mmHg).
Measure heart rate and blood pressure with a tilt-table or active stand test.
Rule out other causes: Dehydration, blood loss, or orthostatic hypotension

Who is affected?

Demographics: Predominantly affects women aged 15-50.
Associated Conditions: Possible after viral infection, trauma, surgery, or pregnancy. This condition is often associated with autoimmune diseases, Ehlers-Danlos syndrome, and CFS.

Management and Treatment

Lifestyle changes:
Increased hydration and salt intake.
Utilize compression stockings for better circulation.
Implement gradual exercise programs such as recumbent cycling and swimming.
Beta-blockers (heart rate reduction).
Fludrocortisone is used to increase blood volume.
Midodrine improves vascular tone.
With no cure, care focuses on symptom control and everyday function.

Risks and Factors Misdiagnosis risk: POTS is commonly misdiagnosed as anxiety, persistent fatigue, or dehydration.

Long-term impact: Can drastically reduce quality of life, although not life-threatening.
Research gaps: The cause of POTS is uncertain, and ongoing investigations are exploring autoimmune and genetic factors.

Can POTS be cured?

There is no cure for POTS. Many people see significant improvement with lifestyle modifications, medications, and physical training, and some symptoms may disappear.

Can POTS Go Away?

No standard treatment eliminates POTS permanently.
Proper care can reduce symptoms and perhaps induce remission. Some individuals with POTS experience symptoms for a lifetime, while others may improve after months or years, particularly if their symptoms developed following a viral illness or surgery.

Medications:

Beta-blockers (lower heart rate).
Increase blood volume using fludrocortisone.
Midodrine promotes vascular tone.
Ivabradine (Corlanor) could reduce tachycardia without lowering blood pressure off-label.

POTS symptoms

Standing upright causes POTS symptoms, including rapid heartbeat, dizziness, fainting, weariness, and “brain fog.” These symptoms range in severity and may have an impact on daily life.

Key Symptoms of POTS:

Cardiovascular:
Rapid heartbeat within 10 minutes of standing
Palpitations or pounding heart, Chest discomfort, Neurological:
Dizziness or lightheadedness, Syncope or near-fainting episodes, Concentration issues (brain fog)
Headaches

General/Systemic:

Excessive weariness and exercise intolerance
Leg weakness • Nausea, bloating, or abdominal pain • Sweating irregularities
Other features:
Symptoms intensify in hot weather due to heat intolerance.
Acrocyanosis (bluish staining of feet/hands when standing) • Sleep disruptions

Symptom Causes

• Prolonged standing (queues, showers, cooking) • Heat exposure (summer weather, hot baths) • Dehydration • Stress or illness • Sudden postural changes

Causes

Autonomic nerve system failure causes Postural Orthostatic Tachycardia Syndrome (POTS), which affects heart rate and blood flow when standing. It commonly follows viral infections, autoimmune diseases, trauma, or genetic connective tissue problems.

The main causes and contributing factors are:

1. ANS dysfunction

The autonomic nervous system fails to regulate blood vessel constriction and heart rate adequately.
Excessive tachycardia occurs when standing, without the typical blood pressure decline of orthostatic hypotension.

2. Abnormal blood volume

Patients with hypovolemia may have lower circulating blood volume.
The legs and abdomen may experience blood pooling, resulting in decreased blood return to the heart and compensatory tachycardia.

3. Autoimmune Links

POTS is linked to autoimmune illnesses such as lupus, Sjögren's syndrome, and Hashimoto's thyroiditis.
Autoantibodies can disrupt autonomic nerve signals.

4. Genetic/Connective Tissue Disorders

Ehlers-Danlos syndrome (EDS): Weak connective tissue causes excessive blood pooling.
Familial predisposition: Possible hereditary influence.

5. Post-Viral or Post-Traumatic Onset

Patients often experience POTS symptoms after:
Viruses like Epstein-Barr and COVID-19 often cause POTS symptoms.
Surgery, trauma, or pregnancy.

6. Other Contributors

Prolonged bed rest or inactivity might increase signs of deconditioning.
Hormonal factors: Most prevalent in women, suggesting estrogen/progesterone involvement.
Neuropathy may cause POTS by damaging tiny nerve fibers that govern blood vessel constriction.

Key Notes

POTS is multifaceted, with no single etiology explaining all cases.
The cause is generally a combination of autonomic dysfunction, blood pooling, autoimmune activity, and hereditary predisposition.
Knowing the cause helps create personalised treatments, like increasing blood volume for low blood levels, using compression garments for blood pooling, and adjusting the immune system for autoimmune-related POTS

Treating POTS

The video about how PTOS is treated

Lifestyle adjustments, physical training, and drugs to minimize symptoms, including rapid heartbeat, dizziness, and exhaustion, are used to treat Postural Orthostatic Tachycardia Syndrome (POTS). A structured management plan is beneficial for most patients.

Also, read https://www.dysautonomiainternational.org/page.php?ID=30

Main Treatment Methods

1. Lifestyle changes

Hydrate and salt: Increase fluid intake (2-3 litres/day) and dietary sodium (3-10 g/day, under medical advice) to increase blood volume.
Compression Garments: Waist-high stockings or abdominal binders minimize leg blood pooling.
Exercise Therapy: Start with recumbent or semi-reclined exercises (e.g., rowing, swimming, cycling) and graduate to upright activities.
Posture Strategies: Reduce prolonged standing, rise slowly, and utilize physical counter-maneuvers (leg crossing, muscle tensing).

2. Symptom-based Heart Rate Control: • Beta-blockers (e.g., propranolol, metoprolol) are recommended.

Ivabradine (off-label, decreases heart rate without reducing blood pressure)
Support for blood pressure and circulation:
Fludrocortisone (blood volume increase)
Midodrine (increases blood vessel tightness and standing tolerance)
Autonomic Modulation:
SSRIs and SNRIs are used to treat anxiety and autonomic dysfunction.
Pyridostigmine (boosts parasympathetic activity)

3. Physiotherapist-supervised graded exercise regimens enhance cardiovascular fitness.

Begin with horizontal workouts and gradually graduate to upright training.

4. Helpful Things

Adjusted diet: Smaller, frequent meals to prevent postprandial symptoms.
Ensure temperature management by avoiding hot situations and showers.
Sleep hygiene: Restful sleep enhances autonomic stability.

Risks and Factors

Each patient responds differently to therapies, requiring individualized programs.
Side effects of medications: Beta-blockers may induce weariness, fludrocortisone may increase blood pressure, and midodrine may cause goosebumps or urinary retention.
POTS misdiagnosis: Commonly misdiagnosed as worry or persistent exhaustion, delaying treatment.
Long-term prognosis: Although treatment often results in improvement, relapses are possible.

Life expectancy with POTS

Chronic, non-fatal Postural Orthostatic Tachycardia Syndrome (POTS) rarely shortens life. Most patients have a favorable long-term outlook, even if it can produce severe symptoms like COPD or congestive heart failure.

Conclusion

Postural Orthostatic Tachycardia Syndrome, a complicated, multivariate autonomic nervous system illness, mostly affects young women but can impact anyone. It causes dizziness, weariness, palpitations, and cognitive issues due to an irregular heart rate spike when standing. POTS is controllable, not curable, and many individuals regain independence and stability with proper treatment.

Perioral Dermatitis: A Guide to Cure the Skin

Describe Perioral dermatitis.

Chronic inflammatory perioral dermatitis creates a red, bumpy rash around the lips, sometimes spreading to the nose and eyes. It manifests as clusters of tiny papules or pustules over redness and scaling and is often associated with topical steroid usage, cosmetics, or skin irritants.

Key Perioral Dermatitis Features

The condition is characterised by a scaly, flaky, red rash accompanied by pustules. It may involve the nose, eyes, and forehead. Particularly the lips. The skin may experience burning, itching, or tightness. Vermillion borders are frequently spared by the rash.

Causes and Risks

Most common trigger: topical corticosteroids.
Heavy cosmetics and moisturisers can clog pores.
Use fluoridated toothpaste or dental products.
Hormonal changes can occur due to the use of oral contraceptives, for example.
Environmental factors include UV exposure and stress.
Rare triggers, such as chewing gum, have been reported.

How does perioral dermatitis look?

Small red lumps, occasionally with pus, surrounded by inflammatory, flaky, or scaly skin around the mouth, nose, or eyes, are typical of perioral dermatitis. The vermillion border of the lips is generally spared, distinguishing the rash from other disorders.

Typical Look

Red papules or pustules: Small lumps that resemble acne but are not real pimples.
Background redness: Skin around pimples may appear irritated.
Dryness or scaling: Rashes may have flaky spots.
Distribution: • Mostly around the mouth.
The rash has the potential to affect the nose, chin, or eyes.
Lip sparing: The rash typically does not affect the lip surface.

What causes perioral dermatitis?

Usually induced by topical corticosteroids on the face, perioral dermatitis can also be caused by cosmetics, heavy moisturisers, fluoride toothpaste, hormonal changes, and environmental irritants, including UV exposure or wind. The key to controlling the illness is finding and eliminating these triggers.

Main causes and triggers

Topical corticosteroids
The most common cause. Even moderate OTC hydrocortisone creams can cause it.
Stopping steroids may exacerbate the rash before improving.
Heavy products like balms, oils, primers, and moisturizers can clog pores and cause irritation.
Common offenders include fragrance, essential oils, alcohol-based toners, and harsh scrubs.

Dental products

Use toothpaste that contains fluoride or tartar-control agents.
Strongly flavoured toothpastes (spicy or minty) may cause flares.
Environmental considerations
Sun exposure, wind, and inadequate photoprotection might aggravate symptoms.
Climate change and stress may contribute.
Hormonal factors: Oral contraceptives and hormonal variations might cause flare-ups.
Unusual triggers
Chewing gum is rarely cited as a cause.

Possible Risks

The condition is more common in women aged 20-45.
Skin type: Sensitive or reactive skin enhances sensitivity.
Medical history: History of topical steroids or chronic skin disorders.

Who suffers from perioral dermatitis?

Men and children can get perioral dermatitis, but women between 20 and 45 are most likely.

Standard Affected Groups

Adult women aged 20-45 years are more susceptible to the condition, likely due to their increased use of topical corticosteroids, cosmetics, and hormonal factors.
Children may develop perioral dermatitis if topical steroids are applied to the face.
Men: Rare but possible—often associated with shaving products, steroid creams, or dental irritants.

Possible Risks

Use of topical corticosteroids, even modest hydrocortisone, may pose a risk.
The use of cosmetics, such as moisturizers, makeup, and occlusives, can also pose potential risks.
Dental products such as fluoridated or tartar-control toothpaste are also commonly used.
Hormonal changes can occur due to the use of oral contraceptives and fluctuations in the menstrual cycle.
Environmental factors: UV exposure, wind, and stress.
Skin type: Sensitive or reactive skin enhances sensitivity.

Is perioral dermatitis contagious?

Perioral dermatitis will not spread.

Why Not Contagious

Inflammatory condition: Caused by irritation, steroid usage, or other triggers, not by contagious bacteria, viruses, or fungi.
No person-to-person transmission: It cannot be spread through touch, utensils, or close contact.
Each occurrence is linked to personal characteristics such as skincare products, toothpaste, or hormonal changes.

Important Note:

Although not contagious, it may resemble acne or rosacea, causing confusion. Avoid unneeded worry and improper treatment with proper diagnosis.

How is perioral dermatitis diagnosed?

Clinicians diagnose perioral dermatitis by inspecting the skin and asking about topical treatments, medications, and symptoms. No lab test exists.

Diagnosis steps

Medical history

The patient may have a history of long-term or recent use of topical corticosteroids on the face.
Use cosmetics, moisturizers, or fluoridated toothpaste.
Hormonal factors such as oral contraceptives and menstruation may also be present.

Physical examination

Rash around lips, nose, or eyes.
The examination reveals small red papules or pustules on a background of redness and scaling.
The vermillion border (lip edge) is reduced.
Exclusion of other conditions

The absence of comedones (blackheads/whiteheads) in perioral dermatitis rules out acne.

Rosacea causes generalized redness and flushing beyond the perioral area.
Seborrheic dermatitis: skin with oily scales, typically in scalp/nasolabial creases.
Allergic contact dermatitis leads to itching and is connected to certain allergens.
Additional tests are usually not required.
Skin swabs or scrapings can rule out bacterial, fungal, or parasitic infections.
Conduct patch testing for possible allergic contact dermatitis.

Treating perioral dermatitis

The video about how to treat Perioral Dermatitis

Stopping triggers (particularly topical steroids and irritating cosmetics) and employing gentle skin care and topical or oral antibiotics treat perioral dermatitis. Most cases improve within weeks after offending agents are removed.

Treatment Steps:

1. Eliminate Triggers

Stop using topical corticosteroids, including modest hydrocortisone.
Withdrawal may induce a brief flare before recovery.
Avoid heavy cosmetics and occlusive moisturizers (oily creams, thick balms).
Change toothpaste if fluoridated or tartar-control types worsen symptoms.
Reduce irritations: fragrance-heavy products, harsh scrubbing, and alcohol-based toners.

2. Topicals

Metronidazole cream/gel: Anti-inflammatory and antibacterial.
Erythromycin gel: Effective for mild instances.
Use pimecrolimus or tacrolimus as non-steroid options for inflammation.
Some use azelaic acid for its anti-inflammatory qualities.

3. Moderate to Severe Oral Treatments

Tetracycline antibiotics, specifically doxycycline, minocycline, and tetracycline, are commonly used.
These antibiotics are typically recommended for a period of 6–12 weeks.
Macrolides (erythromycin, azithromycin) are available for youngsters and pregnant patients.

4. Skin Support

Use mild, soap-free cleaners.
Apply gentle, non-comedogenic moisturizers as needed.
Avoid over-washing or scrubbing the affected region.
Ensure skin is protected from sun and wind exposure.

Also, read https://torontodermatologycentre.com/perioral-dermatitis/.

Prevention and Long-Term Management

Avoid reusing topical steroids on the face.
Streamline skincare with fewer products, fragrance-free, and hypoallergenic options.
Monitor hormonal effects (oral contraceptives may contribute).
Inform patients that POD is not communicable but may recur if triggers return.

Risks and Factors

Steroid withdrawal flare: Symptoms may temporarily intensify after stopping steroids.
Recurrence: High if triggers are reestablished.
Psychological impact: Visible rash might influence confidence and quality of life.

Overnight perioral dermatitis treatment?

Perioral dermatitis is a persistent inflammatory illness that takes weeks to months to heal, even with treatment. Trying to “get rid of it overnight” might frustrate and worsen the rash if harsh or incorrect therapies are employed.

Not Disappearing Overnight

Inflamed skin needs time to settle down after the removal of triggers.
Steroid withdrawal flare: Symptoms may worsen before lessening after stopping topical steroids.
Timeline for treatment:
Topical therapies: 2-4 weeks of improvement.
Oral antibiotics: 4-8 weeks of improvement.

Do It Now

It won't go away overnight, but you can start healing:

Stop topical steroids unless advised by a doctor.
Simplify skincare by using light cleansers and avoiding heavy creams, oils, and makeup.
Avoid fluoridated or tartar-control toothpaste if suspected as a cause.
Avoid irritants like scents, scrubs, and alcohol-based toners.
If outdoors, use light, non-comedogenic sunscreen to protect skin.

Conclusion

Patient and constant treatment are needed to treat perioral dermatitis, an inflammatory reaction. While avoiding triggers and commencing medical treatment is the fastest way to improve, outcomes take time.

Management relies on delicate skin care, avoiding steroids and irritants, and medical treatment as necessary. Preventing recurrence and reducing suffering requires patient education.