Macular Degeneration - Hyperexcision

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Last updated: November 13, 2024Bookmark

Table Of Contents

Overview
Dry Macular Degeneration
Wet Macular Degeneration

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 AMD	Features	Frequency	Progession of symptoms
Dry (geographic) AMD	Associated with drusen (yellow cholesterol-based debris) between the RPE and choroid	80%	Slowly progressive
Wet (exudative) AMD	Associated with neovascularization of the choroid, leading to hemorrhage, ischemia, and scarring. It is more severe and progressive	10-15%	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
- Age (esp. 60+)
- Hypertension
- Obesity
- Elevated cholesterol
- Caucasian
- Smoking
- UV exposure
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

ACTH	P: <80 ng/L
ALT	P: 5–35 U/L
Albumin	P: 35–50 g/L
Aldosterone	P: 100–500 pmol/L
Alk. phosphatase	P: 30–130 U/L
α-Amylase	P: 0–180 IU/dL
α-Fetoprotein	S: <10 kU/L
Angiotensin II	P: 5–35 pmol/L
ADH	P: 0.9–4.6 pmol/L
AST	P: 5–35 U/L
Bicarbonate	P: 24–30 mmol/L
Bilirubin	P: 3–17 μmol/L
BNP	P: <50 ng/L
CRP	P: <10 mg/L
Calcitonin	P: <0.1 mcg/L
Calcium (ionized)	P: 1.0–1.25 mmol/L
Calcium (total)	P: 2.12–2.60 mmol/L
Chloride	P: 95–105 mmol/L
Cholesterol	P: <5.0 mmol/L
VLDL	P: 0.128–0.645 mmol/L
LDL	P: <2.0 mmol/L
HDL	P: 0.9–1.93 mmol/L
Cortisol AM	P: 450–700 nmol/L
Cortisol Midnight	P: 80–280 nmol/L
CK ♂	P: 25–195 U/L
CK ♀	P: 25–170 U/L
Creatinine	P: 70–100 μmol/L
Ferritin	P: 12–200 mcg/L
Folate	S: 2.1 mcg/L
FSH	P: 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 hormone	P: <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
LDH	P: 70–250 U/L
LH	P: 3–16 U/L
Magnesium	P: 0.75–1.05 mmol/L
Osmolality	P: 278–305 mosmol/kg
PTH	P: 0.8–8.5 pmol/L
Potassium	P: 3.5–5.3 mmol/L
Prolactin ♂	P: <450 U/L
Prolactin ♀	P: <600 U/L
PSA	P: 0–4 mcg/mL
Protein (total)	P: 60–80 g/L
Red cell folate	B: 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
Sodium	P: 135–145 mmol/L
TBG	P: 7–17 mg/L
TSH	P: 0.5–4.2 mU/L
T4	P: 70–140 nmol/L
Free T4	P: 9–22 pmol/L
TIBC	S: 54–75 μmol/L
Triglycerides	P: 0.50–2.3 mmol/L
T3	P: 1.2–3.0 nmol/L
Troponin T	P: <0.1 mcg/L
Urate ♂	P: 210–480 μmol/L
Urate ♀	P: 150–390 μmol/L
Urea	P: 2.5–6.7 mmol/L
Vitamin B12	S: 0.13–0.68 nmol/L
Vitamin D	S: 50 nmol/L

Arterial Blood Gases

pH	7.35–7.45
PaCO₂	4.7–6.0 kPa
PaO₂	>10.6 kPa
Base excess	±2 mmol/L

Urine

Cortisol (free)	<280 nmol/24h
Hydroxyindole acetic acid	16–73 μmol/24h
Hydroxymethylmandelic acid	16–48 μmol/24h
Metanephrines	0.03–0.69 μmol/mmol cr.
Osmolality	350–1000 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
Potassium	14–120 mmol/24h
Protein	<150 mg/24h
Protein/creatinine ratio	<3 mg/mmol
Sodium	100–250 mmol/24h

Haematology

WCC	4.0–11.0 ×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
MCV	76–96 fL
MCH	27–32 pg
MCHC	300–360 g/L
RDW	11.6–14.6%
Neutrophils	2.0–7.5 ×10⁹/L (40–75%)
Lymphocytes	1.0–4.5 ×10⁹/L (20–45%)
Eosinophils	0.04–0.44 ×10⁹/L (1–6%)
Basophils	0–0.10 ×10⁹/L (0–1%)
Monocytes	0.2–0.8 ×10⁹/L (2–10%)
Platelets	150–400 ×10⁹/L
Reticulocytes	0.8–2.0% / 25–100 ×10⁹/L
Prothrombin time	10–14 s
APTT	35–45 s

Paediatric

Pulse Rate (bpm)
Neonate	140–160
Infant <1yr	120–140
1–5 years	110–130
5–12 years	80–120
>12 years	70–100
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)
Term	65/45
1 year	75/50
4 years	85/60
8 years	95/65
10 years	100/70
Weight Formulas
3–12 months	(a + 9)/2 kg
1–6 years	2a + 8 kg
>6 years	(7a − 5)/2 kg
Haemoglobin (g/dL)
Term newborn	13–20
1 month	11–18
2 months	10–15
1–2 years	10–13
>2 years	11–14
MUAC (6 months–5 years)
Obese	>17.5 cm
Normal	13.5–17.4 cm
At risk	12.5–13.4 cm
Moderate malnutrition	11.5–12.4 cm
Severe malnutrition	<11.5 cm
Developmental Milestones
Social smile	1.5 months
Head control	4 months
Sits unsupported	7 months
Crawls	10 months
Stands unsupported	10–12 months
Walks	12–13 months
Talks	18 months
CSF WBC (/mm³)
Term newborn	0–25
>2 weeks	0–5

Calculator ›

Overview

Dry Macular Degeneration

Wet Macular Degeneration

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