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Diabetes Mellitus Diagnosis

DM ƒ 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
ƒ Thirst ƒ Frequently asymptomatic nd
ƒ Asymptomatic individuals require a 2 positive reading on a
ƒ Polyuria ƒ Chronic fatigue separate day
ƒ Nocturia ƒ Malaise ƒ Immediate dx in the presence of DKA or HHNK
ƒ Rapid LOW
Impaired Glucose ƒ Fasting plasma glucose <7.0mmol/L AND
ƒ Uncontrolled diabetes may present with increased susceptibility to infections (boils, genital Tolerance (IGT) ƒ Post 75g OGTT 2h plasma glucose 7.8-11.0 mmol/L
candidiasis, pruritus vulvae or balanitis)
Impaired Fasting ƒ Fasting plasma glucose 6.1-6.9 mmol/L AND
Glucose (IFG) ƒ Post 75g OGTT 2h plasma glucose <7.8 mmol/L
Signs GDM ƒ Any degree of glucose intolerance with onset or first recognition
Type I Type II during pregnancy.
ƒ Usually no physical signs - LOW ƒ Overweight / obesity
ƒ DKA – ƒ HPT
- Ketoacidosis: Kussmaul’s breathing, ƒ Hyperlipidaemia ± xanthelasma / Screening of Asymptomatic Individuals
ketotic breath xanthomata ƒ Frequency
- Salt & water depletion: tachycardia, ƒ 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 ƒ Cx of diabetes - Criteria for high risk individual. Screen from 30YO onwards
intraocular pressure - Peripheral neuropathy ƒ Obesity (BMI>27)
- Altered mental state - Glove & stocking paraesthesia ƒ HPT
- Foot ulcer st
ƒ 1 degree relative with DM
- Cataracts / retinopathy ƒ Previous GDM
- Peripheral vascular disease ƒ Coronary artery disease
- Dermopathy - All other individuals to be screened from 40YO onwards.
ƒ 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
ƒ Glucagon
ƒ Cortisol
Fatigue Hyperglycaemia ƒ GH Glycogenolysis ↑
ƒ 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
Treatment (MOH CPG on DM 1999) Initial therapy
Significant hyperglycaemia ƒ Sulphonylurea or Metformin
Aim: Overweight PTs ƒ Metformin (causes weight loss)
ƒ 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
ƒ 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 ƒ Type 1 diabetics
Physical Activity & Exercise ƒ Recommendation: 3-5X / wk, 60-85% max heart rate, 20- ƒ Failure of lifestyle modification and OHGA in glycaemic control in type 2 diabetics
60min each time. Aerobic exercise recommended. ƒ During acute illness or stress for glycaemic control in type 2 diabetics
ƒ Precautions
- Proper footwear Regimen (short acting = Actrapid, long-acting = Insulatard)
- Adequate hydration ƒ 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 ƒ 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
ƒ Prevention of hypoglycaemia insulin; 1/3 of total daily dose in the evening)
- Reduce medication prior to exercise ƒ 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 ƒ Alternatives: Rapid-acting insulin analogues (eg lispro) – not recommended as for now.
- Gradual progression of exercise intensity
- Avoid late night exercise ƒ Type 1 Diabetics: Multiple daily injection or Continuous subcutaneous insulin infusion (CSII)
Smoking cessation ƒ 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 ƒ Hypoglycaemia
ƒ Weight gain
ƒ Peripheral oedema (cause salt and water retention initially when started)
Drugs available
ƒ Insulin antibody
Sulphonylurea ƒ Stimulate pancreatic insulin release ƒ Higher risk of
ƒ Local allergy
ƒ Tolbutamide: short T1/2, gd for elderly hypoglycaemia c.f. other
ƒ Lipodystrophy at injection site
ƒ Chlorpropamide: long T1/2, may cause drugs
prolonged hypoglycaemia. Other SE:
cholestatic jaundice, rash, bld dyscrasia, Monitoring of Blood Glucose Control
SIADH ƒ Self-Monitoring of Blood Glucose (SMBG)
ƒ Glibenclamide: risk of severe - Indications
hypoglycaemia. Avoid in the elderly - All insulin treated PTs (1-2 days per week)
Biguanide ƒ Decrease hepatic gluconeogenesis ƒ GI side effects - Pregnant women with GDM or pregestational DM
(Metformin) ƒ Enhance peripheral glucose uptake ƒ CI in hepatic & renal - Non insulin treated PT with risk of developing hypoglycaemia
ƒ 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 ƒ Slow absorption of starch and sucrose in ƒ GI side effects:
inhibitors the gut by inhibiting disaccharidases. flatulence, bloating,
diarrhoea ƒ Self-monitoring of Urine Glucose
(Acarbose)
- Inaccurate as raised renal threshold for glucose might mask persistent
Thiazolidinediones ƒ Insulin sensitizers ƒ hepatotoxic
hyperglycaemia. Only for PTs unable or unwilling to perform SMBG
(Rosiglitazone) ƒ CI: hepatic impairment
- target control for SMBG:
Repaglinide ƒ Prandial glucose regulator(take b4 meals) ƒ 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

ƒ Self-monitoring of Urine Ketones Prevention of CVS complications


- For type 1 DM, GDM and pregestational diabetes in pregnant women ƒ Main complications: CAD, CVA, PVD
- Indications ƒ Main risk factors to control: HPT, dyslipidaemia, smoking
- Acute illness or stress ƒ 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
ƒ HbA1c CVA)
- Measure of average glycaemia over previous 2-3 months
- Frequency: 3-4mthly in unstable glycaemic control, change in thearpy or failure to ƒ 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
ƒ 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)) ƒ SE: ↑ liver transaminases (check CK and LFT 2-3 mths after starting Rx, stop if
ƒ However, intensive treatment increases the risk of hypoglycaemic events ALT/AST >3X N or CK >10X N), myopathy, rhabdomyolysis
ƒ Therefore, targets must be individualized to the patient ƒ Target: 2.5 mmol/L
↑ TG Moderate ↑TG: fibrates.
Ideal 4.5-6.4% ƒ Not attainable by most diabetic patients ƒ SE: cholesterol gallstone dz, myopathy, ↑CK (rhabdomyolysis), ↑ liver enzymes
ƒ 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% ƒ Desired target for diabetic PTs
Mixed Drug of choice depend on predominant lipid abN
ƒ Increased risk of hypoglycaemia
Suboptimal 7.1-8.0% ƒ Attainable for most diabetic PTs Statin + fibrate combination usually used
Unacceptable >8.0% ƒ Risk of acute metabolic decompensation &/or Cxs of ↓ HDL Fibric acid defivatives.
hyperglycaemia Target: 1.0 mmol/L
ƒ Requires reassessment & readjustment of therapy. 3) Cardiovascular events
+ macrovascular dz Low dose aspirin (100-300 mg/day)
ƒ Most diabetics should aim for ‘Optimal’ control. No macrovascular dz Antiplatelet agents. Check for CI (allergy, blding tendencies, recent
ƒ 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
Prevention of Renal Complications Diabetic Foot Complications
ƒ Main risks: ulcers & LL amputations
ƒ Diabetic nephropathy (DN) accounts for 40% of PTs starting renal dialysis in S’pore ƒ Major cause of disability & mortality
ƒ Type 1 DM usually presents with Microalbuminuria 5-15 yrs after onset ƒ Screening: at dx & annually.
ƒ Type 2 DM usually presents already with overt proteinuria ƒ Wagner’s Classification:
ƒ Rate of decline in GFR = 2-20ml/min/year. a. At risk for lower extremity amputation
ƒ Screening for Microalbuminuria b. Not at risk for lower extremity amputation

Dipstix test Risk factors for lower limb amputation


ƒ Type 1: annually after 5YO Previous ƒ Hx of prev. ulceration
ƒ Type 2: at dx Ulceration
PVD ƒ pedal pulses absent ƒ absence of gradual temp.
ƒ intermittent claudication / gradient
rest pain ƒ absence of hair
Dipstix + Dipstix – Peripheral ƒ negative Semmes- ƒ negative turning fork
st
ƒ 24h UTP ƒ Random daytime / 1 void neuropathy Weinstein 5.07 (128kHz) sensation
ƒ Creatinine clearance urine for alb: creatinine ratio monofilament sensation ƒ paraesthesia or
ƒ negative pin prick anaesthesia
sensation
Diabetic ƒ callus ƒ interdigital maceration
Positive Negative dermopathy ƒ ingrown / mycotic toenails ƒ fissuring esp at heels
ƒ Repeat 2X over 3mths. Microalb. ƒ Repeat test annually ƒ neglect / poor foot ƒ skin &/or tinea pedis
dxed if 2 of 3 samples are positive hygiene infection
Foot deformity ƒ gross foot deformity ƒ Charcot changes
ƒ bunions (rockerbottom foot)
* Dipstix only detects > 200mg/L albumin, ƒ flat feet ƒ Claw, hammer, mallet,
ƒ Intervention to limit progression to not microalbuminuria ƒ high arched feet retracted toes
overt nephropathy ƒ Abnormal gait
ƒ Monitor UTP or microalb every 6-12 Poor footwear ƒ Slippers, flip-flops, thongs ƒ Abnormal wear patterns
mths ƒ Tight or ill fitting shoes

Management:
DM neph: ƒ Optimal glycaemic control
Stage I: glomeular hyperfiltration ƒ Smoking cessation
Stage II: microalbuminemia (>30 mg/d)
Stage III: preoteinuria (>300mg/d)—irreversible from here onwards Not at risk Primary med practitioner & ƒ Screening of foot
Stage IV: renal impairment (Cr >200) diabetic foot care nurse ƒ DM footcare education
Stage V: ESRF (Cr >900)—start preparing for dialysis when Cr ~>500 At risk Specialist footcare team ƒ Wound debridement
ƒ Pressure analysis
ƒ Management: ƒ Orthoses / insoles for pressure distribution
Glycaemic control ƒ Aim for HbA1c <7% ƒ Footwear adaptations
BP control ƒ Aim for <130/80mmHg ƒ DM footcare education
ƒ For those with over nephropathy w proteinuria >1g/day, aim for
<125/75mmHg
st
ƒ 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 ƒ Management:
- Yearly follow-up if no retinopathy, shorter interval depending on severity if
ƒ Leading cause of blindness in adults in S’pore retinopathy present
ƒ DRP likely in the presence of albuminuria and neuropathy (microvascular Cxs) - Optimal glycaemic control
ƒ Type 1 DM: 25% at 5yrs, 97.5% after 15 yrs of DM - HPT control
ƒ Type 2 DM: 28.8% at 5 yrs, 77.8% at 15 yrs of DM - Lipid control
- Smoking cessation
ƒ Classification of DRP - Sight-threatening DRP: laser photocoagulation, occasionally vitretomy
Non-Proliferative Mild/moderate NPDR ƒ Microaneurysms only
Retinopathy (Background diabetic ƒ 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
ƒ Microaneurysms cotton wool spots NPDR Mild/moderate None
ƒ Hard exudates Severe NPDR (Pre- One of the following: Severe/ very severe Consider scatter laser
ƒ Cotton wool spots proliferative diabetic ƒ Retinal hemorrhages or PDR Non high-risk & high-risk Scatter laser w/o delay
ƒ Retinal h’age retinopathy) microaneurysms in 4 quadrants
Advanced Scatter laser w/o delay
ƒ Venous beading ƒ Venous beading in 2 quadrants
Non-resorbing vitreous opacities, traction retinal Vitreous surgery
ƒ Intraretinal microvascular
detachment threatening or involving the macula,
abnormalities in 1 quadrant
combined rhegmatogenous & traction retinal
Very severe NPDR ƒ 2 or more signs of severe
detachment or progressive fibro-proliferative DRP
(Severe pre-proliferative retinopathy
diabetic retinopathy
Proliferative Non high-risk PDR ƒ 1-2 of the following:
Retinopathy ƒ new vessels
(PDR) ƒ new vessels at or near the optic
ƒ neovascularization disk
ƒ vitreous h’age ƒ moderate or severe new vessels
(>1/4 disk area)
ƒ vitreous hemorrhage
High-risk PDR ƒ 3 or more of the features above
Advanced PDR ƒ extensive neovascularisation,
vitreous hemorrhage or fibro-
vascular proliferation with or w/o
retinal detachment
Clinically ƒ any of the following
Significant Macular ƒ thickening of the retina at or w/in 500 microns of the centre of the
Edema (CSME) macula
ƒ retinal thickening ƒ hard exudates at or w/in 500microns of the centre of the macula,
ƒ hard exudates if associated with thickening of the adjacent retina
ƒ 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

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

Symptoms
Autonomic activation ƒ Sweating ƒ Pallor
ƒ Trembling ƒ Hunger
ƒ Tachycardia ƒ Anxiety
Neuroglycopenia ƒ Confusion ƒ Inability to concentrate
ƒ Drowsiness ƒ Incoordination
ƒ Speech difficulty ƒ Seizures
ƒ Focal neuro deficits
Non-specific ƒ Nausea ƒ Headache
ƒ 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
ƒ Absolute or relative decrease in insulin level in the presence of excess glucagon. 5) IV volume replacement
ƒ Usually in type 1 DM First hr NS 15-20 ml/kg/h (~1-1.5L)
ƒ 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)
ƒ Causes When S. glucose < 14mmol/L Change to Paeds D/S (D5W/0.45% NS)
o Infections ƒ Monitor urine output hourly
o Infarction – MI, CVA, GIT, peripheral vasculature ƒ Check U/E/Cr/Glu, beta-hydroxybutyrate & venous pH q2-4 hrs
o Insufficient insulin ƒ 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

ƒ 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
+ + + +
ƒ 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 ± ƒ Give NaHCO3 only if severe hyperkalaemia or arterial pH <7.0 (hydration and
renal ischaemia & oliguria insulin will help correct less severe metabolic acidosis)
ƒ Potassium depletion: ƒ 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 ƒ 0.1 units/kg/hr (5unit/hr in 50kg PT), adjust to obtain
ƒ Clinical features infusion rate of drop in S. glucose by 3-4 mmol/L/hr.
Symptoms Signs ƒ Monitor blood glucose hrly
ƒ Polyuria ƒ N/V ƒ Dehydration ƒ Acetone breath When blood glucose ƒ Halve IV SI infusion rate to 0.05-0.1 units/kg/hr & add
ƒ Polydipsia ƒ Cramps ƒ Hypotension ƒ Hypothermia <14mmol/L dextrose in IV fluid
ƒ LOW ƒ Blurred vision ƒ Tachycardia ƒ Confusion / ƒ Aim for bld glucose level of 8-12 mmol/L
ƒ Weakness ƒ Abdo pain ƒ Kussmaul breathing drowsiness / coma ƒ Maintain SI infusion until acidosis clears
*raised amylase w/o pancreatitis & leukocytosis due to stress reaction common
9) Treat precipitating factor
ƒ Complications 10) Admit
ƒ Cerebral oedema: treat with ƒ Thromboembolism 11) Admit MICU if hypotensive/oliguric & refractory to initial rehydration, mental
mannitol & oxygen ƒ DIVC obtundation/coma or total serum osmolarity >340mOsm/kg
ƒ ARDS ƒ Acute circulatory failure 12) Monitoring
ƒ Cardiac failure H/C Aim for rate of When H/C <14mmol/L
q1hr decrease of 3- ƒ Halve IV SI infusion rate to 0.05-0.1 units/kg/hr
ƒ Management 4mmol/L/hr ƒ 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 ƒ start SCSI q4hr
ƒ U/E/Cr/Ca/Mg/PO4/Glucose ƒ FBC ƒ stop SI infusion after overlap of SCSI of 1 hr
ƒ Urinalysis for ketones & leucocytes ƒ DIC screen if septic
ƒ Urine dipstick ƒ Blood culture
ƒ Serum Ketones (beta- ƒ CXR
hydroxybutyrate) ƒ Cardiac enzymes
ƒ ABG ƒ ECG
Hyperosmolar Hyperglycaemic Non-Ketotic state (HHNK)
ƒ 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

ƒ 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
ƒ Thromboembolic Cxs common: prophylactic SC heparin may be required

ƒ 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
ƒ FBC
ƒ U/E/Cr/Ca/Mg/PO4
ƒ Serum osmolality
ƒ ABG
ƒ Urinalysis
4) Look for cause – ECG, CXR
5) Urine catheter – monitor urine output
6) IV Volume replacement
Significant tissue ƒ NS rapid bolus until perfusion improves & BP stabilizes
st
hypoxia ƒ 1L NS w/in 1 hr, another 1L over nxt 2 hrs
ƒ Then 1 L 0.45% NS over nxt 4 hr
Hypertensive or sig. ƒ 0.45% NS
+
hyperNa (>155mmol/L) ƒ when S. glucose reaches 16mmol/L, switch to IV D5W
+
7) K replacement – same as DKA
8) Monitoring
9) Insulin administration
ƒ Insulin infusion 0.1 units/kg/hr
ƒ 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- ƒ Halve IV SI infusion rate to 0.05-0.1 units/kg/hr University, School of Medicine,
H/C reads 4mmol/L/hr ƒ 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