This document provides information on the diagnosis, symptoms, signs, screening, and treatment of diabetes mellitus. It defines the main types of diabetes as type 1, type 2, gestational diabetes, and prediabetes conditions. It outlines the diagnostic criteria and recommendations for screening asymptomatic individuals. Signs and symptoms of diabetes as well as potential complications are described. Treatment aims and options including lifestyle modifications, oral hypoglycemic agents, and insulin therapy are summarized. The document also discusses prevention and management of diabetes complications focused on cardiovascular, renal, foot, and eye health.

1. Diabetes Mellitus Diagnosis
DM Symptomatic with one of the following
- Casual plasma glucose ≥ 11.1mmol/L
Symptoms: - Fasting plasma glucose ≥ 7.0 mmol/L
Type I Type II
- Post 75g OGTT 2h plasma glucose ≥ 11.1 mmol/L
Thirst Frequently asymptomatic nd
Asymptomatic individuals require a 2 positive reading on a
Polyuria Chronic fatigue separate day
Nocturia Malaise Immediate dx in the presence of DKA or HHNK
Rapid LOW
Impaired Glucose Fasting plasma glucose <7.0mmol/L AND
Uncontrolled diabetes may present with increased susceptibility to infections (boils, genital Tolerance (IGT) Post 75g OGTT 2h plasma glucose 7.8-11.0 mmol/L
candidiasis, pruritus vulvae or balanitis)
Impaired Fasting Fasting plasma glucose 6.1-6.9 mmol/L AND
Glucose (IFG) Post 75g OGTT 2h plasma glucose <7.8 mmol/L
Signs GDM Any degree of glucose intolerance with onset or first recognition
Type I Type II during pregnancy.
Usually no physical signs - LOW Overweight / obesity
DKA – HPT
- Ketoacidosis: Kussmaul’s breathing, Hyperlipidaemia ± xanthelasma / Screening of Asymptomatic Individuals
ketotic breath xanthomata Frequency
- Salt & water depletion: tachycardia, Necrobiosis lipoidica diabeticorum (usually - High risk individuals w N glucose tolerance: 3 yearly screening
hypotension, loss of skin turgor, furred on pre-tibial surface of LL) - Individuals w IFG or IGT: annual screening
tongue, cracked lips, reduced Cx of diabetes - Criteria for high risk individual. Screen from 30YO onwards
intraocular pressure - Peripheral neuropathy Obesity (BMI>27)
- Altered mental state - Glove & stocking paraesthesia HPT
- Foot ulcer st
1 degree relative with DM
- Cataracts / retinopathy Previous GDM
- Peripheral vascular disease Coronary artery disease
- Dermopathy - All other individuals to be screened from 40YO onwards.
Method: rapid capillary blood glucose by glucometer. Do a formal venous blood glucose
Lack of insulin test if:
- Fasting CBG >6.0 mmol/L
- Casual CBG ≥ 7.8 mmol/L
↓ anabolism ↑ secretion of: ↑ catabolism
Glucagon
Cortisol
Fatigue Hyperglycaemia GH Glycogenolysis ↑
catecholamines Gluconeogenesis ↑ Wasting
Lipolysis ↑ LOW
Vulvitis Glycosuria
Balanitis
Hyperketonaemia
Polyuria Osmotic diuresis
Polydipsia Hyperventilation
Tachycardia Salt & water Acidosis Peripheral
↓BP depletion vasodilatation
DKA
Hypotension
Death Hypothermia

2. 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

3. 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
Self-monitoring of Urine Ketones Prevention of CVS complications
- For type 1 DM, GDM and pregestational diabetes in pregnant women Main complications: CAD, CVA, PVD
- Indications Main risk factors to control: HPT, dyslipidaemia, smoking
- Acute illness or stress Investigations & examination:
- Persistent elevated blood glucose >14 mmol/L - Annual screen for dyslipidaemia
- Symptoms of ketoacidosis (N/V, abdo pain, acetone breath) - Annual ECG, BP, BMI
- Examination for PVD, femoral bruit (↑ risk of cardiovas dz) & carotid bruit (↑ risk of
HbA1c CVA)
- Measure of average glycaemia over previous 2-3 months
- Frequency: 3-4mthly in unstable glycaemic control, change in thearpy or failure to Management:
meet target. 6mthly in stable glycaemic control 1) Hypertension
Aim: < 130/80 mmHg
Rx: Choice of drug depends on additional benefits eg renal & cardioprotective effects
Targets of Glycaemic Control
Intensive blood glucose control reduce risk of microvascular disease in PTs with type 1 2) Dyslipidaemia
or 2 diabetes (Diabetes Control & Complications Trial (DCCT) & UK Prospective ↑ LDL HMG-CoA reductase inhibitor (statin)
Diabetes Study (UKPDS)) SE: ↑ liver transaminases (check CK and LFT 2-3 mths after starting Rx, stop if
However, intensive treatment increases the risk of hypoglycaemic events ALT/AST >3X N or CK >10X N), myopathy, rhabdomyolysis
Therefore, targets must be individualized to the patient Target: 2.5 mmol/L
↑ TG Moderate ↑TG: fibrates.
Ideal 4.5-6.4% Not attainable by most diabetic patients SE: cholesterol gallstone dz, myopathy, ↑CK (rhabdomyolysis), ↑ liver enzymes
Desired target for pregnant women with GDM or
Severe ↑TG: combination fibrate with omega-3 polyunsat. fatty acid
pregestational diabetes
Target: 1.7 mmol/L
Optimal 6.5-7.0% Desired target for diabetic PTs
Mixed Drug of choice depend on predominant lipid abN
Increased risk of hypoglycaemia
Suboptimal 7.1-8.0% Attainable for most diabetic PTs Statin + fibrate combination usually used
Unacceptable >8.0% Risk of acute metabolic decompensation &/or Cxs of ↓ HDL Fibric acid defivatives.
hyperglycaemia Target: 1.0 mmol/L
Requires reassessment & readjustment of therapy. 3) Cardiovascular events
+ macrovascular dz Low dose aspirin (100-300 mg/day)
Most diabetics should aim for ‘Optimal’ control. No macrovascular dz Antiplatelet agents. Check for CI (allergy, blding tendencies, recent
Indications for ‘Suboptimal’ target levels (generally PTs at risk of permanent injury from GI bld, active hepatic dz)
hypoglycaemia):
- Older PTs with significant atherosclerosis
- PTs with severe DM Cx or comorbidities (severe CAD, CVA, renal failure,
proliferative retinopathy, advanced autonomic neuropathy)
- Preadolescent children: unpredictable food intake and activity level, poor
compliance to treatment

4. Prevention of Renal Complications Diabetic Foot Complications
Main risks: ulcers & LL amputations
Diabetic nephropathy (DN) accounts for 40% of PTs starting renal dialysis in S’pore Major cause of disability & mortality
Type 1 DM usually presents with Microalbuminuria 5-15 yrs after onset Screening: at dx & annually.
Type 2 DM usually presents already with overt proteinuria Wagner’s Classification:
Rate of decline in GFR = 2-20ml/min/year. a. At risk for lower extremity amputation
Screening for Microalbuminuria b. Not at risk for lower extremity amputation
Dipstix test Risk factors for lower limb amputation
Type 1: annually after 5YO Previous Hx of prev. ulceration
Type 2: at dx Ulceration
PVD pedal pulses absent absence of gradual temp.
intermittent claudication / gradient
rest pain absence of hair
Dipstix + Dipstix – Peripheral negative Semmes- negative turning fork
st
24h UTP Random daytime / 1 void neuropathy Weinstein 5.07 (128kHz) sensation
Creatinine clearance urine for alb: creatinine ratio monofilament sensation paraesthesia or
negative pin prick anaesthesia
sensation
Diabetic callus interdigital maceration
Positive Negative dermopathy ingrown / mycotic toenails fissuring esp at heels
Repeat 2X over 3mths. Microalb. Repeat test annually neglect / poor foot skin &/or tinea pedis
dxed if 2 of 3 samples are positive hygiene infection
Foot deformity gross foot deformity Charcot changes
bunions (rockerbottom foot)
* Dipstix only detects > 200mg/L albumin, flat feet Claw, hammer, mallet,
Intervention to limit progression to not microalbuminuria high arched feet retracted toes
overt nephropathy Abnormal gait
Monitor UTP or microalb every 6-12 Poor footwear Slippers, flip-flops, thongs Abnormal wear patterns
mths Tight or ill fitting shoes
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

5. 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
Eye examination schedule (fundal photography, indirect ophthalmoscopy with slit-lamp
or direct ophthalmoscopy through dilated pupils)
st
1 examination Routine minimum F/U
Type 1 DM w/in 3-5 yrs of dx Yearly
Type 2 DM At diagnosis Yearly
st
Pregestational DM Prior to conception & during Depends on 1 trimester
st
1 trimester screening

6. Hypoglycaemia
Venous blood glucose <3.0 mmol/L a/w typical S&S relieved upon correction of bld Morbidity of severe hypoglycaemia
glucose CNS Coma Brain damage
Usually in diabetic pts treated with insulin or sulphonylureas Convulsions Impaired cognitive function
TIA/Stroke Intellectual decline
Causes Heart Arrhythmias MI
Missed / delayed / inadequate meals Alcohol / salicylates / β-blockers Eye Vitreous hemorrhage Worsening of DRP
Gastroparesis Other endocrine disorders – GH & Others Hypothermia Accidents
Unexpected / unusual exercise cortisol insufficiency
Deficient glucose counter-regulation Sepsis & shock
Impaired awareness of hypoglycaemia Infection
Poorly designed insulin regimen Liver failure / congenital metabolism
Factitious disorders
Errors in OHGA / insulin dose / schedule Cardiac failure
Renal failure
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.

7. 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 6) Early Potassium replacement
+ +
1) Hyperglycaemia Blood glucose ≥14mmol/L S. K < 3.3 mmol/L Give 20-40 mmol K per hr until K+ >3.3mmol/L
2) Hyperketonaemia Ketonaemia or ketonuria (can be given as 2/3 KCl & 1/3 KHPO4 when S. PO4 is
3) Metab acidosis Arterial pH <7.3, bicarbonate <15mmol/L <0.3mmol/L)
+ +
S. K 3.3-4.9 mmol/L Give 10-15 mmol K per hr
+ + + +
Dehydration: usually about 4-6 L, due to osmotic diuresis. a/w loss of Na & K S. K > 5.0 mmol/L Check S. K every 2 hrs, hold off K+ infusion
+ + +
o K loss due to displacement of intracellular K by H
o Fluid deficit initially from intracellular compartment. Later, depletion of 7) Restore acid-base balance
extracellular fluid result in haemoconcentration, hypovolaemia, & hypotension ± Give NaHCO3 only if severe hyperkalaemia or arterial pH <7.0 (hydration and
renal ischaemia & oliguria insulin will help correct less severe metabolic acidosis)
Potassium depletion: IV 8.4% NaHCO3 50-100ml in 200-400ml sterile water over 1-2 hrs (=50-
o Plasma concentration a poor indicator of total deficit. 100mmol). Repeat in 2 hrs if necessary.
+
o Drop in K will occur after starting insulin Rx due to dilution by IV fluids, 8) Insulin administration
+ +
movt of K into ICF and continued renal K loss. Bolus IV SI 0.15 units/kg
Low dose continuous 0.1 units/kg/hr (5unit/hr in 50kg PT), adjust to obtain
Clinical features infusion rate of drop in S. glucose by 3-4 mmol/L/hr.
Symptoms Signs Monitor blood glucose hrly
Polyuria N/V Dehydration Acetone breath When blood glucose Halve IV SI infusion rate to 0.05-0.1 units/kg/hr & add
Polydipsia Cramps Hypotension Hypothermia <14mmol/L dextrose in IV fluid
LOW Blurred vision Tachycardia Confusion / Aim for bld glucose level of 8-12 mmol/L
Weakness Abdo pain Kussmaul breathing drowsiness / coma Maintain SI infusion until acidosis clears
*raised amylase w/o pancreatitis & leukocytosis due to stress reaction common
9) Treat precipitating factor
Complications 10) Admit
Cerebral oedema: treat with Thromboembolism 11) Admit MICU if hypotensive/oliguric & refractory to initial rehydration, mental
mannitol & oxygen DIVC obtundation/coma or total serum osmolarity >340mOsm/kg
ARDS Acute circulatory failure 12) Monitoring
Cardiac failure H/C Aim for rate of When H/C <14mmol/L
q1hr decrease of 3- Halve IV SI infusion rate to 0.05-0.1 units/kg/hr
Management 4mmol/L/hr Change IV fluid to D5W/0.45%NS 1pint q1-4hr
1) Supplemental high-flow O2 Then aim to maintain H/C of 8-12 mmol/L
+
2) Monitoring: ECG, pulse oximetry, vital signs q15min, blood glucose, ketones, K & acid- Labs U/E/Cr/Glu, beta- Monitor K+, ketonaemia and metab acidosis
base balance q1-2hrs q2- hydroxybutyrate & When acidosis clear (pH >7.3 & HCO3 >15)
3) Lab – assess DKA & look for cause 4hrs venous pH start SCSI q4hr
U/E/Cr/Ca/Mg/PO4/Glucose FBC stop SI infusion after overlap of SCSI of 1 hr
Urinalysis for ketones & leucocytes DIC screen if septic
Urine dipstick Blood culture
Serum Ketones (beta- CXR
hydroxybutyrate) Cardiac enzymes
ABG ECG

8. Hyperosmolar Hyperglycaemic Non-Ketotic state (HHNK)
C.f DKA: clinical course runs into days rather than hours, and there is greater fluid (6-
+
10L) and K loss. PTs are usually more sensitive to insulin, thus less insulin is required
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