Appendix 8a
Features of hypoglycaemia in children and the elderly
Children Elderly
Autonomic Hunger trembling pallor Sweating shaking pounding heart anxiety
Neuroglycopenic Dizziness poor concentration drowsiness weakness Weakness drowsiness poor concentration dizziness confusion light headedness
Behavioural Tearful confused tired irritable aggressive
Neurological Unsteady poor co-ordination double vision blurred vision slurred speech
Appendix 8b
General Instructions for Use

The diluent is provided for use only in the preparation of glucagon for parenteral injection and for no other use.

Glucagon should not be used at concentrations greater than 1 mg/ mL (1 unit/ mL).

Reconstituted glucagon should be used immediately. Discard any unused portion.

Reconstituted glucagon solutions should be used only if they are clear and of a water-like consistency.

Parenteral drug products should be inspected visually for particulate matter and discoloration prior to administration.

Directions for Treatment of Severe Hypoglycemia

Severe hypoglycemia should be treated initially with intravenous glucose, if possible.

If parenteral glucose can not be used, dissolve the lyophilized glucagon using the accompanying diluting solution and use immediately.

For adults and for pediatric patients weighing more than 44 lb (20 kg), give 1 mg (1 unit) by subcutaneous, intramuscular, or intravenous injection.

For pediatric patients weighing less than 44 lb (20 kg), give 0.5 mg (0.5 unit) or a dose equivalent to 20- 30 µg/ kg.

Discard any unused portion.

An unconscious patient will usually awaken within 15 minutes following the glucagon injection. If the response is delayed, there is no contraindication to the administration of an additional dose of glucagon; however, in view of the deleterious effects of cerebral hypoglycemia, emergency aid should be sought so that parenteral glucose can be given.

After the patient responds, supplemental carbohydrate should be given to restore liver glycogen and to prevent secondary hypoglycemia.

Appendix 9a

Consider feet to be "at risk" if patient cannot feel the 10gm monofilament at any of the sites marked.

Appendix 9b
Arsenic poisoning
B12 deficiency
Cancer (paraneoplastic syndromes)
Carpal tunnel and other entrapment syndromes
Chacot marie tooth Disease
Guillian Barre Syndrome
Heavy metal poisoning
Herpes zoster
HIV/AIDS-related neuropathies
Myaesthenia gravis
Peripheral vascular disease
Vasculitic polyneuropathy

Drug related: Alcohol, amiadirone, colchicines, dapsone, hydralazine, isoniazid, metronidalzole, nitrofurantoin, phenytoin, pyridoxine, statins, sulfasalazine;

Appendix 11a
  1. A more rapid decrease in the GFR than is expected.
  2. Sudden development of nephrotic syndrome.
  3. Absence of retinopathy.
  4. Presence of hematuria ; although red cell casts have been described in some patients.
  5. Renal bruit.
  6. Absent pedal pulses.
  7. Disproportionately high serum potassium.
  8. Sudden deterioration in renal function after starting Ace inhibitors.
  9. Presence of cardiac failure, and the use of drugs, like diuretics, in its management.
  10. Testing after heavy exercise.
  11. Testing during acute illness.
  12. High protein intake.
  13. Decompensation of metabolic control, including recent ketosis.
Appendix 12 a
Stage Physical Changes Functional Changes


Moderately severe to very severe non-proliferative diabetic retinopathy is also known as pre-proliferative diabetic retinopathy.


Stage of microaneurisms (bulging vessels) tiny retinal blood vessels. These changes are visible only in an eye exam, when the pupils are dilated.


Some blood vessels that nourish the retina are blocked. Small bleeds may occur on the surface of the retina.


Most individuals perceive no vision changes.

Macular edema, if present, should be considered a medical sight threatening emergency.

As more vessels are blocked, parts of the retina are deprived of blood supply and set the stage of new blood vessels to be formed to supply these parts.

If vessels begin to leak, the leaking fluid and lipid may collect in the macula, a condition called "macular edema."

Macular edema can occur at any stage of diabetic retinopathy and should be considered a medical emergency.


Areas with blocked vessels show the growth of thin walled and fragile new vessels which take an abnormal course across the retina. (neovascularisation).

These vessels can break and bleed into the vitreous, preventing light from reaching the retina.

Scar tissue may also form near the retina, detaching it from the back of the eye and resulting in blindness.

Fluid in the vitreous and/or macular edema may also be present.

Spotty or cloudy vision, double vision, reduced vision, dark or floating spots.

In late stages, severe vision loss may occur leading to "legal" blindness in the affected eye(s).

Macular edema, if present, should be considered a medical sight threatening emergency.

Appendix 12 b
  1. Look at the square (grid).
  2. Wear your reading glasses (if you use one) and cover one eye.
  3. Focus on the center dot for one full minute.
  4. While looking directly at the center, be sure that all the lines are straight and clear, and all the small squares are the same size.
  5. Repeat the test in the other eye.
  6. If any lines or squares appear distorted, wavy, blurred, discolored, or otherwise abnormal, call your eye doctor right away.
  7. In healthy eyes the lines are straight.

The Amsler's chart is very useful for early detection of macular problems and thus is very important as this may be an early sign of macular problems and lead to a loss of central vision! But one must know its limitations. The Amsler grid will NOT detect proliferative diabetic retinopathy, most preproliferative changes and other types of damage that may threaten vision, nor is it useful for detecting any of the early changes. Remember: a normal Amsler grid test does not rule out the presence of retinopathy that can threaten your vision. It cannot replace routine eye exams. Only regular eye exams can do this.