Diamond-Blackfan anemia (DBA) is a rare congenital blood disorder characterized by the failure of the bone marrow to produce red blood cells. It usually presents in infancy and is classified as a congenital pure red cell aplasia. DBA is notable for its genetic basis, variable physical malformations, and lifelong management challenges.

Key facts

• Onset: Typically within the first year of life
• Genetic cause: Mutations in ribosomal protein genes
• Inheritance pattern: Autosomal dominant (most cases de novo)
• Prevalence: About 5–7 per million live births
• Treatment options: Corticosteroids, chronic transfusions, or stem cell transplantation

Pathophysiology

Diamond-Blackfan anemia arises from mutations that impair ribosome biogenesis, leading to defective erythroid progenitor development. The bone marrow becomes selectively deficient in red cell precursors, while white cells and platelets remain normal. Most cases involve mutations in genes encoding ribosomal proteins such as RPS19, RPL5, or RPL11, disrupting protein synthesis and cellular growth.

Clinical features

Infants with DBA commonly present with pallor and anemia. Physical anomalies are present in about half of cases, including craniofacial abnormalities, thumb or limb malformations, and heart or kidney defects. Growth retardation and an increased lifetime risk of malignancies such as leukemia and osteogenic sarcoma are recognized complications.

Diagnosis

Diagnosis combines hematologic findings—macrocytic anemia, reticulocytopenia, and normal marrow cellularity except for absent red cell precursors—with genetic testing for ribosomal protein gene mutations. Elevated erythrocyte adenosine deaminase (eADA) activity is a common biomarker.

Management and prognosis

Initial treatment often involves corticosteroids to stimulate red cell production. Patients unresponsive to steroids may require regular transfusions with iron chelation therapy to prevent overload, or hematopoietic stem cell transplantation as a potential cure. Advances in genetic understanding have improved prognosis, but lifelong monitoring remains essential due to treatment complications and cancer risk.

(A Scientific, Myth-Busting Blog with Visual Explanation)

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Introduction

This is one of the most common myths people believe:
👉 “Regular sex makes breasts and butt bigger.”

It sounds believable—because sex involves hormones, body changes, and physical stimulation. But what does actual medical science say?

Let’s break it down with evidence.

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What Happens to the Body During Sex?

7

During sexual arousal and orgasm, several temporary physiological changes occur:

Increased blood flow

• Blood vessels dilate (vasocongestion)
• Breasts may appear fuller and slightly enlarged

Hormonal release

• Oxytocin, dopamine, estrogen, progesterone rise
• Nipples become erect and more sensitive

Temporary swelling effect

• Breasts can appear 15–25% larger during arousal

👉 But here’s the key:
These changes are temporary and reverse after sex.

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Does Sex Cause Permanent Breast Growth?

Short answer: No.

Scientific evidence clearly shows:

• Breast size is mainly determined by:
  • Genetics
  • Body fat
  • Hormonal changes (puberty, pregnancy, medications)
• Sex does NOT cause permanent breast enlargement

Even repeated sexual activity does not stimulate long-term tissue growth.

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What Actually Increases Breast Size?

6

Real, evidence-based factors:

1. Genetics

• The biggest determinant of size and shape

2. Body weight / fat

• Breasts are largely fatty tissue
• Weight gain → size increase

3. Hormones

• Estrogen & progesterone drive growth
• Seen during:
  • Puberty
  • Pregnancy
  • Hormonal therapy

4. Pregnancy & lactation

• Causes true enlargement due to glandular growth

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What About Buttocks Size?

6

Does sex increase butt size?

No — not directly.

Buttocks size depends on:

• Fat distribution (influenced by estrogen)
• Muscle mass (gluteal muscles)
• Genetics
• Exercise (e.g., squats, hip thrusts)

Sex does not stimulate fat deposition or muscle growth in the buttocks.

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Why Do People Believe This Myth?

Several reasons:

1. Temporary swelling during sex

• Breasts look bigger → mistaken as permanent

2. Hormonal timing confusion

• Women may notice changes during:
  • Ovulation
  • Menstrual cycle
• These are hormone-driven, not sex-driven

3. Cultural myths

• Similar to:
  • “Marriage increases breast size” (also false)

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Final Scientific Verdict

What sex DOES do:

• Temporary breast fullness
• Nipple erection
• Increased sensitivity
• Short-term hormonal fluctuations

What sex DOES NOT do:

• Permanently increase breast size
• Increase butt size
• Change body fat distribution

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Clinical Bottom Line (For Medical Perspective)

• Breast size = fat + glandular tissue + hormones
• Butt size = fat distribution + muscle mass
• Sex = transient physiological response only

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Conclusion

Sex may make breasts look bigger for a short time, but it does not cause real growth.
Butt size is completely unrelated to sexual activity.

This is a classic biological myth—explained by temporary changes and misunderstood hormones.

A structured, practical guide for clinicians

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Introduction

Vomiting is one of the most common presenting complaints in pediatric practice—ranging from benign, self-limiting illnesses to life-threatening surgical and metabolic emergencies. It is not a diagnosis, but a symptom with a broad differential, involving gastrointestinal (GI), neurological, metabolic, infectious, and psychological causes.

The real challenge is not treating vomiting—but identifying which child is sick and why.

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Understanding Vomiting

Vomiting is a protective reflex involving coordinated contraction of abdominal muscles and relaxation of the lower esophageal sphincter, leading to expulsion of gastric contents.

Types of Vomiting

• Acute vomiting → hours to days (e.g., gastroenteritis)
• Chronic vomiting → weeks (e.g., GERD, metabolic causes)
• Cyclic vomiting → episodic with symptom-free intervals
• Projectile vomiting → suggests obstruction (e.g., pyloric stenosis)
• Bilious vomiting (green) → surgical emergency until proven otherwise

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Step 1: Initial Stabilization (ABC First)

Before thinking of diagnosis:

• Airway → risk of aspiration
• Breathing → respiratory distress?
• Circulation → shock, dehydration

Assess:

• Vitals
• Capillary refill
• Level of consciousness
• Hydration status

👉 This step is critical because vomiting can rapidly lead to dehydration and electrolyte imbalance.

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Step 2: Identify RED FLAG Signs

These determine urgency and need for immediate intervention:

Major Red Flags

• Bilious (green) vomiting
• Bloody vomiting
• Altered sensorium
• Severe dehydration
• Persistent projectile vomiting
• Abdominal distension or peritonitis
• Inconsolable crying (infants)
• Neck stiffness + fever (meningitis)
• Morning vomiting + headache (raised ICP)

These features suggest serious pathology such as:

• Intestinal obstruction
• Intussusception
• Meningitis
• Intracranial hypertension
• Appendicitis

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Step 3: Age-Based Differential Diagnosis

Age is one of the most powerful diagnostic clues.

1. Neonates (0–28 days)

Think danger first:

• Intestinal obstruction (atresia, malrotation)
• Hirschsprung disease
• Sepsis
• Inborn errors of metabolism

👉 Bilious vomiting = surgical emergency

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2. Infants

• Gastroesophageal reflux (common)
• Pyloric stenosis → projectile vomiting
• Intussusception
• Food allergy
• Infection

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3. Children

• Acute gastroenteritis (most common)
• Appendicitis
• UTI
• Pneumonia (post-tussive vomiting)
• Migraine

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4. Adolescents

• Pregnancy
• Eating disorders
• Drug/toxin ingestion
• Diabetic ketoacidosis (DKA)
• Intracranial causes

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Step 4: Focused History

A good history often gives the diagnosis.

Key Questions

1. Onset
   • Sudden → infection, obstruction
   • Chronic → GERD, metabolic
2. Character of Vomit
   • Bilious → obstruction
   • Projectile → pyloric stenosis
   • Blood → gastritis, ulcer
3. Relation to Feeding
   • Immediately after feeds → reflux
   • Delayed → obstruction
4. Associated Symptoms
   • Fever → infection
   • Diarrhea → gastroenteritis
   • Headache → intracranial cause
   • Abdominal pain → surgical cause
5. Systemic Clues
   • Poor weight gain → chronic disease
   • Polyuria → DKA
   • Drug ingestion → toxins

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Step 5: Physical Examination

General Examination

• Hydration status:
  • Sunken eyes
  • Dry mucosa
  • Reduced urine output

• Growth parameters (failure to thrive?)

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Systemic Examination

Abdomen

• Distension → obstruction
• Tenderness → appendicitis
• Mass → intussusception

CNS

• Bulging fontanelle (infants)
• Neck stiffness
• Altered consciousness

Skin

• Rash → infection/allergy
• Petechiae → sepsis

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Step 6: Investigations

👉 No “routine panel” exists — investigations should be targeted.

Basic Investigations

• Serum electrolytes
• Blood glucose
• Blood gas (if severe)

When Indicated

• Imaging
  • X-ray abdomen → obstruction
  • Ultrasound → intussusception
  • CT/MRI → CNS causes
• Other tests
  • Urine analysis → UTI
  • LFT/RFT → systemic disease
  • Metabolic screening

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Step 7: Management Approach

1. Treat the Cause (Definitive)

• Surgery → obstruction
• Antibiotics → infection
• Insulin → DKA

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2. Correct Dehydration (MOST IMPORTANT)

Mild–Moderate:

• Oral Rehydration Therapy (ORT)

Severe:

• IV fluids (bolus + maintenance)

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3. Symptomatic Treatment

• Ondansetron for persistent vomiting
• NG decompression in obstruction
• Electrolyte correction

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4. Nutritional Support

• Early feeding when tolerated
• Continue breastfeeding

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Step 8: Clinical Patterns to Recognize (Exam Gold)

Pattern	Likely Diagnosis
Projectile, non-bilious	Pyloric stenosis
Bilious vomiting	Intestinal obstruction
Vomiting + diarrhea	Gastroenteritis
Vomiting + headache (morning)	Raised ICP
Vomiting + abdominal pain → later	Appendicitis
Episodic vomiting, symptom-free intervals	Cyclic vomiting

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Common Pitfalls

• Ignoring bilious vomiting
• Missing appendicitis early
• Assuming all vomiting = gastroenteritis
• Not checking hydration status
• Over-ordering unnecessary tests

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Clinical Algorithm (Simple Mental Model)

1. Is the child sick? (ABC + red flags)
2. What is the age?
3. What is the type of vomiting?
4. What are associated symptoms?
5. Targeted investigations
6. Treat dehydration + cause

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Key Takeaways

• Most pediatric vomiting is benign and self-limiting
• But always rule out life-threatening causes first
• Age + vomiting type + red flags = diagnosis
• Hydration management saves lives

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Conclusion

Vomiting in children is a diagnostic puzzle—but a structured approach simplifies it. The goal is not to memorize hundreds of causes, but to quickly identify danger, localize the system involved, and act appropriately.

1. Definition

GIR (Glucose Infusion Rate) = amount of glucose delivered per kg body weight per minute.

👉 Unit: mg/kg/min

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2. Formula

GIR=Dextrose (%) ×Infusion rate (mL/kg/day)144GIR = \frac{\text{Dextrose (\%) } \times \text{Infusion rate (mL/kg/day)}}{144}GIR=144Dextrose (%) ×Infusion rate (mL/kg/day)​

👉 Alternate (commonly used in ICU):GIR=Dextrose (g/mL)×mL/kg/min×10001GIR = \frac{\text{Dextrose (g/mL)} \times \text{mL/kg/min} \times 1000}{1}GIR=1Dextrose (g/mL)×mL/kg/min×1000​

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3. Normal Glucose Requirement (Term Neonate)

Age	GIR (mg/kg/min)
First 24 hrs	4–6
After 24 hrs	5–8

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4. Treatment of Hypoglycemia

Symptomatic OR RBS <40 mg/dL

Step 1: Bolus

• 10% Dextrose
• Dose: 2 mL/kg IV bolus

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Step 2: Continuous Infusion

Severity	Starting GIR
Mild	4–6 mg/kg/min
Moderate	6–8 mg/kg/min
Severe/refractory	8–12 mg/kg/min

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5. Escalation Strategy

• Increase GIR by 2 mg/kg/min every 30–60 min
• Max GIR: 12–15 mg/kg/min (sometimes up to 20 in refractory cases)

👉 If still hypoglycemic:

• Consider:
  • Sepsis
  • Hyperinsulinism
  • Endocrine causes

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6. Practical Conversion Table

GIR (mg/kg/min)	D10 Rate (mL/kg/day)
4	60
5	75
6	90
8	120
10	150

👉 Quick memory:
D10 @ 80–100 mL/kg/day ≈ GIR 5–7

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7. When High GIR Needed (>8–10)

Think:

• Hyperinsulinism
• Sepsis
• Inborn errors of metabolism
• Hypopituitarism
• Adrenal insufficiency

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8. Choice of Dextrose Concentration

Fluid	Use
D10	First-line
D12.5	Peripheral max
D15–D25	Central line only

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9. Monitoring

• RBS every 30–60 min initially
• Then every 4–6 hrs
• Watch for:
  • Rebound hypoglycemia
  • Fluid overload

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10. Weaning

• Reduce GIR gradually once stable (>50–60 mg/dL)
• Start/advance enteral feeds

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Exam Pearls

• First step = D10 bolus (2 mL/kg)
• Target glucose >45 mg/dL
• GIR >8 = suspect pathology
• Max peripheral dextrose = 12.5%
• Persistent hypoglycemia → think hyperinsulinism

1. Definition

Lumbar puncture (LP) is a procedure in which a needle is inserted into the subarachnoid space of the lumbar spine to obtain cerebrospinal fluid (CSF) for diagnostic or therapeutic purposes.

Commonly done at L3–L4 or L4–L5 intervertebral space.

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2. Indications

A. Diagnostic Indications

1. Suspected CNS infection

• Meningitis
  • Bacterial
  • Viral
  • Tubercular
  • Fungal
• Encephalitis
• Brain abscess (supportive)
• Neurosyphilis

2. Neonatal sepsis evaluation

Important in:

• Neonates with positive blood culture
• Sepsis with neurologic signs
• Late onset sepsis
• Persistent unexplained illness

3. Neurologic disorders

• Guillain-Barré syndrome (albuminocytologic dissociation)
• Multiple sclerosis
• Demyelinating diseases
• Leukodystrophy

4. Malignancy

• Leukemia CNS involvement
• Lymphoma
• Medulloblastoma spread

5. Subarachnoid hemorrhage

When CT scan is negative but suspicion persists.

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B. Therapeutic Indications

• Intrathecal chemotherapy
• Intrathecal antibiotics
• Spinal anesthesia
• CSF pressure reduction (rare)

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3. Indications Specific to Neonates

Perform LP in neonates with:

1. Suspected meningitis
2. Positive blood culture
3. Seizures
4. Bulging fontanelle
5. Apnea / unexplained respiratory deterioration
6. Neurological abnormalities
7. Late onset sepsis (>72 hrs)

May delay LP in unstable neonate until stabilization.

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4. Contraindications

Absolute Contraindications

• Signs of raised intracranial pressure with mass lesion
• Cardiorespiratory instability
• Local infection at puncture site

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Relative Contraindications

• Severe thrombocytopenia (<50,000)
• Coagulopathy
• Spinal deformity
• Suspected spinal cord mass
• Severe shock

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5. Signs Suggesting Raised ICP (Do NOT perform LP immediately)

• Focal neurological deficits
• Papilledema
• Altered consciousness
• Unequal pupils
• Abnormal posturing
• Hypertension with bradycardia (Cushing triad)

These require neuroimaging first.

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6. Anatomy

LP is done below the conus medullaris.

Age	Conus level
Neonate	L3
Adult	L1–L2

Safe spaces:

• L3–L4
• L4–L5

Landmark:
Tuffier line (line joining iliac crests) → L4 vertebra

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7. Equipment

• Sterile gloves
• Antiseptic solution
• Sterile drapes
• Spinal needle with stylet
• Manometer
• 3–4 sterile tubes
• Local anesthetic (lidocaine)
• Syringes
• Adhesive dressing

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8. Needle Size

Age	Needle
Neonate	22–25G
Infant	22G
Child	20–22G

Typical length:

• Neonate: 1.5 inch
• Older children: 2.5 inch

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9. Position

1. Lateral decubitus (preferred)

• Knees flexed to chest
• Chin flexed
• Allows opening pressure measurement

2. Sitting position

Used when landmarks difficult.

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10. Procedure Steps

1. Position child
2. Identify L3–L4 or L4–L5
3. Clean with antiseptic
4. Sterile draping
5. Local anesthesia
6. Insert needle midline with stylet
7. Advance slowly
8. Feel “pop” entering subarachnoid space
9. Remove stylet → CSF flows
10. Collect CSF in tubes
11. Replace stylet and remove needle

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11. CSF Collection Tubes

Tube	Test
Tube 1	Biochemistry (protein, glucose)
Tube 2	Microbiology (Gram stain, culture)
Tube 3	Cell count
Tube 4	Special tests (PCR, viral studies)

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12. Opening Pressure

Measured with manometer.

Normal values:

Age	Pressure
Neonates	2–6 cm H₂O
Children	10–28 cm H₂O

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13. Normal CSF Values

Neonates

Parameter	Normal
Cells	0–20/mm³
Protein	40–120 mg/dL
Glucose	2/3 blood glucose

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Infants & Children

Parameter	Normal
Cells	0–5/mm³
Protein	15–45 mg/dL
Glucose	2/3 serum

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14. CSF Interpretation

Bacterial Meningitis

Finding	Result
Cells	↑ (100–10,000)
Cell type	Neutrophils
Protein	↑↑
Glucose	↓
Opening pressure	↑

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Viral Meningitis

Finding	Result
Cells	10–1000
Cell type	Lymphocytes
Protein	Mild ↑
Glucose	Normal

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TB Meningitis

Finding	Result
Cells	50–500
Type	Lymphocytes
Protein	↑↑
Glucose	↓

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15. Complications

Immediate

• Traumatic tap
• Pain
• Bleeding
• Infection

Post LP

• Post-LP headache
• Back pain

Serious

• Brain herniation
• Epidural hematoma
• Nerve injury

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16. Traumatic Tap Differentiation

Feature	Traumatic tap	SAH
RBC count	Decreases in later tubes	Same in all tubes
Clot	Present	Absent
Xanthochromia	Absent	Present

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17. Reasons for Failed LP

• Wrong level
• Poor positioning
• Obesity
• Dehydration
• Needle obstruction

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18. When NOT to Delay Antibiotics

In suspected meningitis:

• Start antibiotics immediately
• LP should not delay treatment

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19. Special Considerations in Neonates

• Higher CSF protein normally
• CSF WBC slightly higher
• LP often required in late onset sepsis
• May be delayed if unstable

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✅ Exam Pearls (Important for MD / Residency)

• Best site: L3–L4
• Neonatal normal CSF protein higher
• Always replace stylet before removing needle
• Opening pressure measured only in lateral position
• Papilledema → neuroimaging before LP