Macular Degeneration

Last updated: November 13, 2024

Overview

Macular degeneration is the most common cause of permanent visual loss in the elderly. It is AKA age-related macular degeneration (AMD). It is a chronic condition that leads to progressive ventral visual loss. The macula is essential for central vision. Degeneration therefore leads to visual disruption causing distortion (metamorphopsia) and loss of central vision (central scotomas).

Its etiology is unknown. It typically presents as an older patient with blurry vision and dark spots that worsen over time. All patients with AMD receive regular followup with optometry. No effective surgical or medical treatment currently exists for dry AMD.

Type of AMDFeaturesFrequencyProgession of symptoms
Dry (geographic) AMDAssociated with drusen (yellow cholesterol-based debris) between the RPE and choroid80%Slowly progressive
Wet (exudative) AMDAssociated with neovascularization of the choroid, leading to hemorrhage, ischemia, and scarring. It is more severe and progressive10-15%Rapidly progressive (over days or weeks)
  • Important relevant anatomy:
    • Bruch’s membrane
      • Innermost layer of the choroid located beneath the retina
    • Retinal pigment epithelium
      • Located in the retina beneath the photoreceptors next to the choroid (Bruch’s membrane)
  • Risk factors
  • Signs and symptoms
    • Blurred central vision
    • Metamorphopsia (distorted vision)
    • Dramatic decrease in visual acuity (affects the ability to read and distinguish faces)
    • Decreased contrast sensitivity
  • Investigations
    • Ophthalmoscopy (indirect and dilated): for definitive diagnosis and differentiation (wet or dry AMD)
    • Snellen chart
      • Reduced visual acuity compared to the previous test
    • Amsler grid
      • Distortion
    • Fluorescein angiography: performed in suspected wet AMD to visualize abnormal blood vessels
      • Areas of bleeding (bright spots) around the macula
How Amsler grid may appear in a patient with AMD. Source- American Academy of Ophthalmologists

Dry Macular Degeneration

This is as a result of the accumulation of drusen. Drusen is yellow extracellular material that forms between Bruch’s membrane and retinal pigment epithelium (RPE). It results in gradual loss of vision. There is no specific treatment. Vitamins and antioxidant supplements may prevent it.

Drusen seen overlying the macula in dry AMD

Drusen is a common finding. The presence of drusen is not pathognomonic for AMD. However, the more drusen the more likely the patient will develop AMD.

Fluorescein angiography showing hyperfluorescence where there is atrophy of the RPE. Source- Medscape

Wet Macular Degeneration

This is caused by a break in Bruch’s membrane. Blood vessels form beneath the retina which later leak and cause haemorrhage. It can progress rapidly to vision loss. Treatments include laser therapy and anti-VEGF medication (e.g. ranibizumab).

  • Treatment summary
    • Dry AMD
      • Refer to an optometrist to facilitate care and improve quality of life
      • Oral vitamins and anti-oxidants: slows progression
    • Wet AMD
      • Photodynamic therapy (PDT): lasers are used to coagulate abnormal vessels and slow the progression
      • Anti-VEGF agents (Bevacizumab, Ranibizumab, Pegaptinib, Zivaflibercept): administered intravitreally q2-4 weeks to antagonize angiogenesis
      • Oral vitamins and anti-oxidants: slows progression
  • How can you improve the safety and Quality of Life for patients with AMD?
    • Keep the home brightly lit
    • Take precautions with stairs
    • Use cane/walker for walking
    • Use objects with larger symbols
    • Use magnification devices
    • Use colour-coded medicine bottles
    • At home care
    • Disability/ADA counselling if they are still working
    • Talking glucometer for patients with Diabetes
Hemorrhaging and scarring as seen in wet AMD. Source- American Academy of Ophthalmoscopy
Reference Intervals
Biochemistry
ACTHP: <80 ng/L
ALTP: 5–35 U/L
AlbuminP: 35–50 g/L
AldosteroneP: 100–500 pmol/L
Alk. phosphataseP: 30–130 U/L
α-AmylaseP: 0–180 IU/dL
α-FetoproteinS: <10 kU/L
Angiotensin IIP: 5–35 pmol/L
ADHP: 0.9–4.6 pmol/L
ASTP: 5–35 U/L
BicarbonateP: 24–30 mmol/L
BilirubinP: 3–17 μmol/L
BNPP: <50 ng/L
CRPP: <10 mg/L
CalcitoninP: <0.1 mcg/L
Calcium (ionized)P: 1.0–1.25 mmol/L
Calcium (total)P: 2.12–2.60 mmol/L
ChlorideP: 95–105 mmol/L
CholesterolP: <5.0 mmol/L
VLDLP: 0.128–0.645 mmol/L
LDLP: <2.0 mmol/L
HDLP: 0.9–1.93 mmol/L
Cortisol AMP: 450–700 nmol/L
Cortisol MidnightP: 80–280 nmol/L
CK ♂P: 25–195 U/L
CK ♀P: 25–170 U/L
CreatinineP: 70–100 μmol/L
FerritinP: 12–200 mcg/L
FolateS: 2.1 mcg/L
FSHP: 2–8 U/L ♂; >25 menopause
GGT ♂P: 11–51 U/L
GGT ♀P: 7–33 U/L
Glucose (fasting)P: 3.5–5.5 mmol/L
Growth hormoneP: <20 mu/L
HbA1C (DCCT)B: 4–6%
HbA1C (IFCC)B: 20–42 mmol/mol
Iron ♂S: 14–31 μmol/L
Iron ♀S: 11–30 μmol/L
Lactate (venous)P: 0.6–2.4 mmol/L
Lactate (arterial)P: 0.6–1.8 mmol/L
LDHP: 70–250 U/L
LHP: 3–16 U/L
MagnesiumP: 0.75–1.05 mmol/L
OsmolalityP: 278–305 mosmol/kg
PTHP: 0.8–8.5 pmol/L
PotassiumP: 3.5–5.3 mmol/L
Prolactin ♂P: <450 U/L
Prolactin ♀P: <600 U/L
PSAP: 0–4 mcg/mL
Protein (total)P: 60–80 g/L
Red cell folateB: 0.36–1.44 μmol/L
Renin (erect)P: 2.8–4.5 pmol/mL/h
Renin (recumbent)P: 1.1–2.7 pmol/mL/h
SodiumP: 135–145 mmol/L
TBGP: 7–17 mg/L
TSHP: 0.5–4.2 mU/L
T4P: 70–140 nmol/L
Free T4P: 9–22 pmol/L
TIBCS: 54–75 μmol/L
TriglyceridesP: 0.50–2.3 mmol/L
T3P: 1.2–3.0 nmol/L
Troponin TP: <0.1 mcg/L
Urate ♂P: 210–480 μmol/L
Urate ♀P: 150–390 μmol/L
UreaP: 2.5–6.7 mmol/L
Vitamin B12S: 0.13–0.68 nmol/L
Vitamin DS: 50 nmol/L
Arterial Blood Gases
pH7.35–7.45
PaCO₂4.7–6.0 kPa
PaO₂>10.6 kPa
Base excess±2 mmol/L
Urine
Cortisol (free)<280 nmol/24h
Hydroxyindole acetic acid16–73 μmol/24h
Hydroxymethylmandelic acid16–48 μmol/24h
Metanephrines0.03–0.69 μmol/mmol cr.
Osmolality350–1000 mosmol/kg
17-Oxogenic steroids ♂28–30 μmol/24h
17-Oxogenic steroids ♀21–66 μmol/24h
17-Oxosteroids ♂17–76 μmol/24h
17-Oxosteroids ♀14–59 μmol/24h
Phosphate (inorganic)15–50 mmol/24h
Potassium14–120 mmol/24h
Protein<150 mg/24h
Protein/creatinine ratio<3 mg/mmol
Sodium100–250 mmol/24h
Haematology
WCC4.0–11.0 ×10⁹/L
RBC ♂4.5–6.5 ×10¹²/L
RBC ♀3.9–5.6 ×10¹²/L
Hb ♂130–180 g/L
Hb ♀115–160 g/L
PCV ♂0.4–0.54 L/L
PCV ♀0.37–0.47 L/L
MCV76–96 fL
MCH27–32 pg
MCHC300–360 g/L
RDW11.6–14.6%
Neutrophils2.0–7.5 ×10⁹/L (40–75%)
Lymphocytes1.0–4.5 ×10⁹/L (20–45%)
Eosinophils0.04–0.44 ×10⁹/L (1–6%)
Basophils0–0.10 ×10⁹/L (0–1%)
Monocytes0.2–0.8 ×10⁹/L (2–10%)
Platelets150–400 ×10⁹/L
Reticulocytes0.8–2.0% / 25–100 ×10⁹/L
Prothrombin time10–14 s
APTT35–45 s
Paediatric
Pulse Rate (bpm)
Neonate140–160
Infant <1yr120–140
1–5 years110–130
5–12 years80–120
>12 years70–100
Respiratory Rate (tachypnoea)
0–2 months≥60/min
2–12 months≥50/min
1–5 years≥40/min
>5 years≥30/min
Blood Pressure (mmHg)
Term65/45
1 year75/50
4 years85/60
8 years95/65
10 years100/70
Weight Formulas
3–12 months(a + 9)/2 kg
1–6 years2a + 8 kg
>6 years(7a − 5)/2 kg
Haemoglobin (g/dL)
Term newborn13–20
1 month11–18
2 months10–15
1–2 years10–13
>2 years11–14
MUAC (6 months–5 years)
Obese>17.5 cm
Normal13.5–17.4 cm
At risk12.5–13.4 cm
Moderate malnutrition11.5–12.4 cm
Severe malnutrition<11.5 cm
Developmental Milestones
Social smile1.5 months
Head control4 months
Sits unsupported7 months
Crawls10 months
Stands unsupported10–12 months
Walks12–13 months
Talks18 months
CSF WBC (/mm³)
Term newborn0–25
>2 weeks0–5
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