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DKA
Hypotension
Death Hypothermia
Treatment (MOH CPG on DM 1999) Initial therapy
Significant hyperglycaemia Sulphonylurea or Metformin
Aim: Overweight PTs Metformin (causes weight loss)
to maintain general health so as to allow the person to live a normal and active live. *α-glucosidase inhibitors: add to diet or other OHGA therapy to improve glucose control, or
avoidance of acute hyper/hypoglycaemic complications and chronic vascular complications. as a monotherapy
A) Lifestyle modification – first line Rx for type 2 diabetics. Attempt for 2-4 mths C) Insulin Therapy
Medical Nutrition Therapy Low saturated fat & cholesterol Indications
Low sodium for individuals with HPT Type 1 diabetics
Physical Activity & Exercise Recommendation: 3-5X / wk, 60-85% max heart rate, 20- Failure of lifestyle modification and OHGA in glycaemic control in type 2 diabetics
60min each time. Aerobic exercise recommended. During acute illness or stress for glycaemic control in type 2 diabetics
Precautions
- Proper footwear Regimen (short acting = Actrapid, long-acting = Insulatard)
- Adequate hydration Multiple daily injections (regular insulin before each meal + intermediate or long acting
- Avoid heavy resistance & isometric exercise insulin as basal insulin)
- Avoid exercise when severly hyperglycaemic or 2 injections per day (mixture of regular & intermediate-acting insulin before breakfast and
hypoglycaemic for Type 1 diabetics dinner – 2/3 of total daily dose in the morning in ratio of 1:2 of short:intermediate acting
Prevention of hypoglycaemia insulin; 1/3 of total daily dose in the evening)
- Reduce medication prior to exercise Single injection of intermediate acting insulin at bedtime + OHGA during the day (for Type
- Consume some CHO 30-60 min before exercise and 2 diabetics only)
after 30 mins of exercise Alternatives: Rapid-acting insulin analogues (eg lispro) – not recommended as for now.
- Gradual progression of exercise intensity
- Avoid late night exercise Type 1 Diabetics: Multiple daily injection or Continuous subcutaneous insulin infusion (CSII)
Smoking cessation Type 2 Diabetics: stepwise therapy with multiple pharmacological therapies needed over
Alcohol Alcohol consumption discouraged time to maintain target glucose control. 2 or more OHGA, or insulin Rx ± OHGA may be
required
Side effects:
B) Pharmacotherapy – when diet & exercise fail to control glycaemia in type 2 diabetics Hypoglycaemia
Weight gain
Peripheral oedema (cause salt and water retention initially when started)
Drugs available
Insulin antibody
Sulphonylurea Stimulate pancreatic insulin release Higher risk of
Local allergy
Tolbutamide: short T1/2, gd for elderly hypoglycaemia c.f. other
Lipodystrophy at injection site
Chlorpropamide: long T1/2, may cause drugs
prolonged hypoglycaemia. Other SE:
cholestatic jaundice, rash, bld dyscrasia, Monitoring of Blood Glucose Control
SIADH Self-Monitoring of Blood Glucose (SMBG)
Glibenclamide: risk of severe - Indications
hypoglycaemia. Avoid in the elderly - All insulin treated PTs (1-2 days per week)
Biguanide Decrease hepatic gluconeogenesis GI side effects - Pregnant women with GDM or pregestational DM
(Metformin) Enhance peripheral glucose uptake CI in hepatic & renal - Non insulin treated PT with risk of developing hypoglycaemia
Delay glucose absorption insufficiency due to risk - All PTs who fail to achieve glycaemic goals
of lactic acidosis - PT education: to interpret results of SMBG and modify Rx accordingly if possible for
optimal benefit.
α-glucosidase Slow absorption of starch and sucrose in GI side effects:
inhibitors the gut by inhibiting disaccharidases. flatulence, bloating,
diarrhoea Self-monitoring of Urine Glucose
(Acarbose)
- Inaccurate as raised renal threshold for glucose might mask persistent
Thiazolidinediones Insulin sensitizers hepatotoxic
hyperglycaemia. Only for PTs unable or unwilling to perform SMBG
(Rosiglitazone) CI: hepatic impairment
- target control for SMBG:
Repaglinide Prandial glucose regulator(take b4 meals) Hypoglycemia
premeal h/c postmeal h/c
ideal (non-DM) 4.0-6.0 5.0-7.0
optimal 6.1-8.0 7.1-10.0
suboptimal 8.1-10.0 10.1-13.0
unacceptable >10.0 >13.0
Management:
DM neph: Optimal glycaemic control
Stage I: glomeular hyperfiltration Smoking cessation
Stage II: microalbuminemia (>30 mg/d)
Stage III: preoteinuria (>300mg/d)—irreversible from here onwards Not at risk Primary med practitioner & Screening of foot
Stage IV: renal impairment (Cr >200) diabetic foot care nurse DM footcare education
Stage V: ESRF (Cr >900)—start preparing for dialysis when Cr ~>500 At risk Specialist footcare team Wound debridement
Pressure analysis
Management: Orthoses / insoles for pressure distribution
Glycaemic control Aim for HbA1c <7% Footwear adaptations
BP control Aim for <130/80mmHg DM footcare education
For those with over nephropathy w proteinuria >1g/day, aim for
<125/75mmHg
st
ACE-I is preferred 1 line drug as it reduces proteinuria and slows
rate of decline of GFR. Check electrolytes 7days after introduction,
and monitor for ↑K+ or ↓ing GFR
Low Protein diet Delay progression of CRF in type 1 diabetics with overt nephropathy
Lipid control Reduce proteinuria and rate of decline in GFR in DN
Smoking Risk factor in devt of DN
Diabetic Retinopathy Management:
- Yearly follow-up if no retinopathy, shorter interval depending on severity if
Leading cause of blindness in adults in S’pore retinopathy present
DRP likely in the presence of albuminuria and neuropathy (microvascular Cxs) - Optimal glycaemic control
Type 1 DM: 25% at 5yrs, 97.5% after 15 yrs of DM - HPT control
Type 2 DM: 28.8% at 5 yrs, 77.8% at 15 yrs of DM - Lipid control
- Smoking cessation
Classification of DRP - Sight-threatening DRP: laser photocoagulation, occasionally vitretomy
Non-Proliferative Mild/moderate NPDR Microaneurysms only
Retinopathy (Background diabetic Mild degree of venous loops, retinal No macular edema None
(NPDR) retinopathy) hemorrhages, hard exudates, Macular edema threatening or involving macular centre Focal / grid macular laser
Microaneurysms cotton wool spots NPDR Mild/moderate None
Hard exudates Severe NPDR (Pre- One of the following: Severe/ very severe Consider scatter laser
Cotton wool spots proliferative diabetic Retinal hemorrhages or PDR Non high-risk & high-risk Scatter laser w/o delay
Retinal h’age retinopathy) microaneurysms in 4 quadrants
Advanced Scatter laser w/o delay
Venous beading Venous beading in 2 quadrants
Non-resorbing vitreous opacities, traction retinal Vitreous surgery
Intraretinal microvascular
detachment threatening or involving the macula,
abnormalities in 1 quadrant
combined rhegmatogenous & traction retinal
Very severe NPDR 2 or more signs of severe
detachment or progressive fibro-proliferative DRP
(Severe pre-proliferative retinopathy
diabetic retinopathy
Proliferative Non high-risk PDR 1-2 of the following:
Retinopathy new vessels
(PDR) new vessels at or near the optic
neovascularization disk
vitreous h’age moderate or severe new vessels
(>1/4 disk area)
vitreous hemorrhage
High-risk PDR 3 or more of the features above
Advanced PDR extensive neovascularisation,
vitreous hemorrhage or fibro-
vascular proliferation with or w/o
retinal detachment
Clinically any of the following
Significant Macular thickening of the retina at or w/in 500 microns of the centre of the
Edema (CSME) macula
retinal thickening hard exudates at or w/in 500microns of the centre of the macula,
hard exudates if associated with thickening of the adjacent retina
areas of retinal thickening 1 disk area or larger, any part of which
is w/in 1 disc diameter of the centre of the macula
Symptoms
Autonomic activation Sweating Pallor
Trembling Hunger
Tachycardia Anxiety
Neuroglycopenia Confusion Inability to concentrate
Drowsiness Incoordination
Speech difficulty Seizures
Focal neuro deficits
Non-specific Nausea Headache
Tiredness
Management
1. Monitoring: ECG, pulse oximetry, vital signs
2. Supplemental low-flow O2
3. Check capillary blood glucose stat
4. Hx & examination: medication hx, recent change in drug / doses, recent & chronic
illnesses
5. Investigations: venous blood glucose, U/E/Cr, LFT, FBC
6. Treatment
Conscious PT Oral carbohydrate rich drink
Unconscious PT IV access available: IV dextrose 50% 40-50ml
No IV access: IM/SC glucagon 1mg (not for hypoglycaemia
due to sulphonylurea or liver failure)
Chronic alcoholism IV thiamine 100mg
Adrenal insufficiency IV hydrocortisone 100-200mg
Associated injuries Tetanus prophylaxis
7. Continued glucose monitoring: capillary blood glucose every 30 mins for first 2 hrs, Digitally signed by DR WANA HLA SHWE
hourly thereafter. DN: cn=DR WANA HLA SHWE, c=MY, o=UCSI
University, School of Medicine, KT-Campus, Terengganu,
8. Persistent altered mental state despite resolution of hypoglycaemia: CT head to exclude ou=Internal Medicine Group, email=wunna.
other causes hlashwe@gmail.com
Reason: This document is for UCSI University, School of
9. Disposition: depends on aetiology, severity, response and comorbidities. Admit all cases Medicine students.
Date: 2009.03.05 09:01:51 +08'00'
due to sulphonylureas due to long half-live of the agent.
Diabetic Ketoacidosis 4) Urinary catheter – monitor urine output
Absolute or relative decrease in insulin level in the presence of excess glucagon. 5) IV volume replacement
Usually in type 1 DM First hr NS 15-20 ml/kg/h (~1-1.5L)
Common presentation: PT devt infection causing LOW and PT stop insulin Rx. Nxt 2-4 hr 0.45% NS 10-20ml/kg/h (~1 pint q1-4 hrly)
Causes When S. glucose < 14mmol/L Change to Paeds D/S (D5W/0.45% NS)
o Infections Monitor urine output hourly
o Infarction – MI, CVA, GIT, peripheral vasculature Check U/E/Cr/Glu, beta-hydroxybutyrate & venous pH q2-4 hrs
o Insufficient insulin Correct fluid deficit (4-6L) w/in first 24 hrs, but serum osmolality should not
o Intercurrent illness drop by > 3 mOsm/kg/hr to prevent cerebral edema
Diagnostic criteria
1 Hyperglycaemia Blood glucose ≥33mmol/L
2 Hyperosmolality S. total osmolality >330mOsm/kg H2O or
effective S. osmolality >320 mOsm/kg H2O*
3 Metab acidosis Arterial pH >7.3, bicarbonate >15mmol/L
4 No ketonaemia or ketouria
+
*Effective S. osmolality = 2XNa + glucose level + urea
** exclude other causes of obtundation if s. osmolality is not high enough
Thromboembolic Cxs common: prophylactic SC heparin may be required
Management
Similar to DKA with certain exceptions
1) Supplemental High-flow O2
+
2) Monitoring: ECG, pulse oximetry, vital signs q15min, blood glucose & K q1-2hrs
3) Labs
FBC
U/E/Cr/Ca/Mg/PO4
Serum osmolality
ABG
Urinalysis
4) Look for cause – ECG, CXR
5) Urine catheter – monitor urine output
6) IV Volume replacement
Significant tissue NS rapid bolus until perfusion improves & BP stabilizes
st
hypoxia 1L NS w/in 1 hr, another 1L over nxt 2 hrs
Then 1 L 0.45% NS over nxt 4 hr
Hypertensive or sig. 0.45% NS
+
hyperNa (>155mmol/L) when S. glucose reaches 16mmol/L, switch to IV D5W
+
7) K replacement – same as DKA
8) Monitoring
9) Insulin administration
Insulin infusion 0.1 units/kg/hr
Adjust to maintain bld glucose at 14-16 mmol/L until S. osmolality ≤315 mOsm/L &
PT is mentally alert Digitally signed by DR WANA
10) Monitoring HLA SHWE
H/C (& venous Aim for rate of When H/C <16mmol/L DN: cn=DR WANA HLA
SHWE, c=MY, o=UCSI
bld glucose if decrease of 3- Halve IV SI infusion rate to 0.05-0.1 units/kg/hr University, School of Medicine,
H/C reads 4mmol/L/hr Change IV fluid to D5W 1pint q1-4hr KT-Campus, Terengganu,
ou=Internal Medicine Group,
“HHH”) Then aim to maintain H/C of 14-16 mmol/L until email=wunna.hlashwe@gmail.
q1 hr plasma osmolarity ≤315mOsm/kg & PT is alert com
Reason: This document is for
Labs U/E/Cr/Glu & Monitor K+, ketonaemia and metab acidosis UCSI year 4 students.
q2-4hrs beta- Date: 2009.02.19 09:28:42
+08'00'
hydroxybutyrate