EcG Nd Diabetics Flashcards

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1
Q

What is DIabetes what May it be due to
When will type 1 be detected
When will type 2 usually be seen
How do you diagnose gestational diabetes

A

It is a chronic metabolic disorder characterized by persistent hyperglycemia.

May be due to impaired insulin secretion, resistance to peripheral actions of insulin, or both.

Type 1 is usually detected incidentally and it’s detected early
Type 2 usually Comes Late and presents w complications

Diagnosed using OGTT cuz there’s impaired fasting blood glucose
It’s diagnosed from second trimester

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2
Q

What are the characteristics of the types of diabetes and the characteristics of gestational diabetes

A

Type 1:

Characterised by autoimmune destruction of insulin-producing beta cells of the pancreas
•Leads to absolute insulin deficiency
•Accounts for 5-10%
•Most commonly seen in children and adolescents (can be at any age)

Type 2:

Defined by insulin resistance.
•Progressive loss of β-cell insulin secretion
•Account for ~90% of all cases
•Most common >45 years (can occur at any age)
•Risks: Obesity, physical inactivity, energy-dense diets

Gestational:

  • Hyperglycaemia first detected in pregnancy
  • Usually occurs in 2nd and 3rd trimesters
  • Complicates 7% of all pregnancies
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3
Q

State the risk factors for type 2 diabetes

Define two other types of diabetes and give two examples of each

A

Family history of Type 2 DM (parent or sibling with Type 2 DM)
•Obesity
•Sedentary lifestyle
•Race/ethnicity (African/Hispanic/Native/Asians)
•Previously identified IFG or IGT
•History of GDM or delivery of baby >4 kg
•Hypertension
•Dyslipidaemia
•Polycystic ovary syndrome or acanthosis nigricans
•History of vascular disease

Monogenic Diabetes
Caused by a single mutation in an autosomal dominant gene
LADA and MOD1

Secondary Diabetes
Due to complications of other diseases

Prednisolone causing diabetes
Endocrine diseases
Auto immune destruction of the pancreas

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4
Q

Name some causes of secondary diabetes

A

Diseases of Exocrine pancreas
•Cystic Fibrosis
•Pancreatitis

  • Drugs or chemicals
  • Glucocorticoid use
  • after organ transplantation,
  • drugs used in the treatment of HIV/AIDS,
  • Thiazide diuretics
  • Phenytoin
  • Associated with genetic syndrome
  • Down Syndrome
  • Klinefelters Syndrome
  • Excess endogenous production of hormonal antagonists to insulin:
  • Growth hormone: acromegaly
  • Glucocorticoid: Cushing’s syndrome
  • Glucagon: Glucagonoma
  • Catecholamines: Phaeochromocytoma
  • Thyroid Hormones: Thyrotoxicosis
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5
Q

How is diabetes diagnosed using FBs,RBS,HbA1C,OGTT

A

FBS of more than 7mmol/L or 126 mg/dL ,checked twice four hours apart
If checked once the patient must have typical signs (weight loss(common in type 1), polyphagia,polydypsia,polyuria )

Or RBs of more than 11.1 mmol/L or 200mg/dL
And HbA1C of more than 6.5 or 48mmol/mol

OGTT:
When fasting your glucose is more than 7mmol/L . Less than 7 is normal
Two hours after taking the glucose your blood level of glucose is more than 11.1mmol/L . Less than 7.8 is normal
Results are from venous plasma cuz whole blood values are lower

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6
Q

Name some supportive investigations
Name four acute complications
Name ten chronic complications
People will present to the emergency with acute complications true or false

A

•Urine microscopy and dipstick: there’s a difference between microscopy and dipstick
Dipstick is a chemistry stick. 30s the lowest and the 120s the highest
Measures glucose,protein,bilirubin,urobilinogen,specific gravity,leukocytes,blood or Haemoglobin ,ketones,pH of urine,nitrite

  • Renal Function Test
  • Liver Function Test
  • ECG(diabetics can come w MI causing the DKA)
  • Cultures when necessary
  • Chest X-ray when indicated
Acute:
Hypoglycemia 
DKA
Hyperglycemic hyperosmolar  non Ketotic state (HHS)
Lactic acidosis 

Chronic:

MICROVASCULAR
•Diabetic Eye Disease
•Diabetic Retinopathy
•Cataract
•External ocular palsies
•Diabetic Nephropathy
•Diabetic Neuropathy

MACROVASCULAR
•Stroke
•Myocardial Infarction
•Peripheral Vascular Disease

  • diabetic foot
  • infections
  • skin and joints problems
    Impotence
    Postural hypotension
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7
Q

What is hypoglycemia
What is the alert value for hypoglycemia in diabetics
And what’s the value for hypo in not al people
State six risk factors for severe hypoglycemia

A

All episodes of an abnormally low plasma glucose concentrations (with or without symptoms) that expose the individual to harm

Alert Value - < 3.9mmol/L or 4
•Clinically important biochemical hypoglycaemia - < 3mmol/

Strict glycaemic control
•Impaired awareness of hypoglycaemia
•Age (very young and elderly)
•Long duration of diabetes
•Sleep
•C-peptide negativity (indicating complete insulin deficiency)
•History of previous severe hypoglycaemia
•Renal impairment(when sugar is going down and proteins are in their urine think of renal impairment. It’s not that the diabetes is cured)
•Genetic, e.g. angiotensin-converting enzyme (ACE) genotype

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8
Q
State the classes of symptoms of hypoglycemia And give the symptoms in each class 
Why don’t most type 2s show autonomic symptoms? 
Which people wont present w autonomic symptoms at all 

Symptoms differ with age; children exhibit behavioural changes (such as naughtiness or irritability), while elderly people experience more prominent neurological symptoms (such as visual disturbance and ataxia true or false

A
Autonomic:
•Sweating
•Trembling
•Pounding heart
•Hunger
•Anxiety
Neuroglycopaenic:
•Confusion
•Drowsiness
•Speech difficulty
•Inability to concentrate
•Incoordination
•Irritability, anger

Nonspecific:
•Nausea
•Tiredness
•Headache

Most type 2s don’t cuz of neuropathy and can jump straight to neuroglycopaenic symptoms

The elderly patients

Symptoms differ with age; children exhibit behavioural changes (such as naughtiness or irritability), while elderly people experience more prominent neurological symptoms (such as visual disturbance and ataxia so true

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9
Q

State six causes of hypoglycemia
Drugs for diabetes oral hypoglycemics and insulin will stay longer in the body if there’s renal impairment true or false

State four ways you can avoid hypoglycemia while traveling

A

Missed, delayed or inadequate meal
•Unexpected or unusual exercise
•Alcohol
•Errors in oral anti-diabetic agent(s) or insulin dose/schedule/administration
•Poorly designed insulin regimen, particularly if predisposing to nocturnal hyperinsulinaemia
•Lipohypertrophy at injection sites causing variable insulin absorption
•Gastroparesis due to autonomic neuropathy causing variable carbohydrate absorption
•Malabsorption, e.g. coeliac disease
•Unrecognised other endocrine disorders, e.g. Addison’s disease
•Factitious (deliberately induced)
•Breastfeeding

Carry a supply of fast-acting carbohydrate (non-perishable in suitable containers)
➢Screwtop plastic bottles or glucose drinks
➢Packets of powdered glucose (for use in hot, humid climates)
➢Confectionery (foil-wrapped in hot climates)
➢Companions should carry additional oral carbohydrate, and glucagon
➢Perform frequent blood glucose testing
➢Carry spare meter and/or visually read strips
➢Use fast-acting insulin analogues for long-distance air travel

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10
Q

How is mild and severe hypoglycemia managed

A

Mild or self treated
•Oral fast-acting carbohydrate (10-15 g) is taken as glucose drink or tablets or confectionery
•Should be followed with a snack containing complex carbohydrate

Severe,external help will be required :

  • If patient is semiconscious or unconscious; parenteral treatment is required
  • IV 75ml 20% dextrose = 15 g OR
  • Give 0.2g/kg in children
  • IM glucagon 1mg (0.5mg in children)
  • If patient is conscious and able to swallow
  • Give oral refined glucose as drink or sweets = 25 g OR
  • Apply glucose gel or jam or honey to buccal mucosa
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11
Q

What is DKA
Under what circumstances will it occur
When can DKA occur in type 2s

A

It is the hallmark of Type 1 DIabetes(insulin deficiency)

Previously underdiagnosed DM
•Interruption of insulin therapy
•The stress of intercurrent illness

in situations of relative insulin deficiency. So in type 2 there’s a state of relative insulin deficiency where insulin receptors don’t respond to insulin anymore as the disease progresses making DKA likely to occur

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12
Q

What are the clincial manifestations of DKA (history and exam)
What are the five principles of DKA management

A
History
•Failure to comply with insulin therapy
•Generalised weakness
•Rapid weight loss (newly diagnosed)
•Symptoms of infection (fever, dysuria etc)
Examination
•Signs of shock
•Pulse: >100bpm or <60bpm
•Systolic Bp<90 mmHg
•GCS <12
•O2 saturation <92%
•Look for infection
Fluid replacement 
Replacement of deficient insulin
Replacement of electrolyte losses
Restore acid base balance
Look for underlying cause
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13
Q

How is DKA diagnosed
How will bicarbonate show if there’s DKA
What’s the most common precipitatant of DKA
When will urinary ketones be negative in DKA

A

H yperglycaemia
•Measure blood glucose
•Ketonaemia
•Test plasma with Ketostix (if available)
•Finger-prick sample for β-hydroxybutyrate
•Ketonuria
•Measure urine ketone levels where plasma ketone measurements are not available
•Acidosis: measure
•pH in arterial blood
•Bicarbonate in venous blood

Bicarbonate can be measured on RFT.
It’s high in alkalosis and low in acidosis so it’ll be low if there’s DKA

Common include infections,dehydration, infarction

They’ll be negative if the patient w DKA presents early so in this case repeat again after six hours to check if ketones are in the urine

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14
Q

What do you do immediately if there’s DKA

A

1.Asses
2.Send bloods to laboratory
3.Set up i.v infusion
•Blood glucose
•Measure baseline and hourly initially
•Aim for fall of 3-6mmol/L (55-110mg/dL) per hour
•Urea and electrolytes
•Perform at baseline and hourly until 6 hours, then at 12 hours and 24 hours
•Potassium: add when K+ <3.5 mmol/L. Give 20 mmol/h in infusion. 10mmol/h when K+ = 3.5-5 mmol/L
•Full blood count
•Blood gases: at 0, 2 hours, 6 hours
•Creatinine: at 0, 6, 12, 24 hours
•Bicarbonate: at 0, 1, 2, 3, 6, 12, 24 hours

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15
Q

What is done in phase 1 management of DKA

A
Admit to HDU(high dependency unit)
•Insulin
•Soluble insulin i.v 0.1 u/kg/h by infusion
•Fluid and Electrolyte Replacement:
•IV 0.9% NaCl with 20 mmol KCl/L
•1 L in 30min, then
•1 L in 1 h
•1 L in 2 h
•1 L in 4 h
•1 L in 8 h
•Adjust KCl concentration depending on results of regular blood K+ measurement

If Blood pressure below 80 mmHg, give 500 mL 0.9% NaCl over 15mins; if no response, give plasma expander
•pH below 7.0 give 500 mL of NaCl 1.26% plus 10mmol KCl. Repeat if necessary to bring pH up to 7.0

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16
Q

What is done in phase 2 management and phase three
I’m phase three you’re finding the cause of the DKA
True or false
How can you differentiate DKA and HHS

A

Insulin and Glucose
•When blood glucose falls to 10-12 mmol/L, change infusion fluid to 1 L 5% glucose plus 20 mmol KCL 6-hourly.
•Continue insulin with dose adjusted according to hourly blood glucose test results (e.g. i.v. 3 U/h glucose 15 mmol/L; 2 U/h when glucose 10 mmol/L

Once stable and able to eat and drink normally, transfer patient to four times daily subcutaneous insulin regimen (based on previous 24 hours’ insulin consumption and trend consumption).
•Other semi-urgent procedures
•Blood and urine culture
•Cardiac enzymes
•Chest X-ray
•ECG
•Monitor if electrolyte problems or severe DKA
•Catheterisation if no urine passed after 3 hours of hydration
Give antibiotics if there’s infection

True

Using Urine dipstick
Bicarbonate levels can be used to differentiate the two

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17
Q

What special measures are done in the management of DKA

A

Broad-spectrum antibiotic if infection likely
➢Bladder catheter if no urine passed in 2 hours
➢Nasogastric tube if drowsy
➢Consider CVP pressure monitoring if shocked or if previous cardiac or renal impairment
➢Give s.c. prophylactic LMW heparin

Subsequent management:

Monitor glucose hourly for 8 hours
➢Monitor electrolytes 2-hourly for 8 hours
➢Adjust K replacement according to results

18
Q

What is HHS
What does the patient usually present w
I’m HHS there’s no acidosis and no ketosis true or false
What should you pay attention to in HHS
In both DKA and HHS the patient is very dehydrated true or false
HHS patients usually come comatose and because of the hyperosmolarity there’s an increased chance of clotting

A

Severe hyperglycaemia without significant ketosis

Typical of Type 2 DM (rarely Type 1)

Patients presents in Mid Middle or Later Life often with previously undiagnosed Diabetes

True
Electrolyte changes

19
Q

State the electrolyte and their values in Severe DKA and HHS
Sodium,potassium,chloride,bicarbonate,urea,glucose,arterial pH

A

Na+ (mmol/L)
Severe DKA :140
HHS: 155

K+ (mmol/L)
5
5

Cl- (mmol/L)
100
110

HCO3- (mmol/L)
5
25

Urea (mmol/L)
8
15

Glucose (mmol/L)
30
50

Arterial pH

  1. 0
  2. 35
20
Q

How is HHS managed
When will you use 0.45 percent NaCl
When will you initiate Insulin IV infusion

A

Measure or calculate serum osmolality frequency
Give fluid replacement with 0.9 NaCl
-•Use 0.45% NaCl only if osmolality is increasing, despite positive fluid balance
•Target fall in plasma sodium is ≤ 10mmol/L at 24 hrs
hrs

Aim for positive fluid balance of 3-6 L by 12 hrs, and replacement of remaining estimated loss over next 12 hrs

Initiate insulin 1V infusion (0.05 U/kg BW/hr) only when blood glucose is not falling with 0.9% NaCl alone OR if there is significant ketonaemia (3β-hydroxybutyrate >1 mmol/L or urine ketones >2+).
-Reduce blood glucose by no more than 5 mmol/L/hr

Treat coexisting conditions

Give prophylactic anticoagulation

21
Q

When will you know if you’ve given fluid overdose
Insulin is very important in DKA cuz if insulin deficiency and they usually come w acute kidney injury
What is lactic acidosis
How will you manage it

A

If person has pulmonary edema

Elevation of lactate and hydrogen ions due to
•Overproduction
•Delayed clearance
•Or a combination of both
•Blood lactate > 5 mmol/L (normal 0.4-1.2mmol/L)
•Types
•Type A
•Type B
•Metformin-associated

Supportive care at ICU
Bicarbonate therapy
Discuss w specialist

22
Q

What is electrocardiogram

What are the properties of the SA node,AV node and bundle of HIs (their bpm and importance)

A

Electrocardiogram
•It assesses the conduction system of the Heart

SA NODE
60 – 100
Situated in the upper part of the wall of the right atrium. It is the heart’s natural pacemaker
AV NODE
40 – 60
It connects the atria and the ventricles. Controls the heart rate. Takes impulses from the SA and send its to the ventricle
BUNDLE OF HIS
20 – 40
Transmits impulses from the AV Node. Located in the AV Septum. Distributes impulses to the ventricles through the purkinje fibres

23
Q

In a normal PQRST,what does P wave,PR interval,QRS complex,ST segment represent?,what’s their duration,shape,height,orientation

A
P wave represents atrial depolarization 
Duration of less than 0.12 second
Height is less than 2.5 mm
Shape is smooth
Orientation,it’s positive in leads I,II,aVF,V4,
Negative in aVR

PR wave:
Atrial depolarization and delay at the AV node (AV conduction time)
Duration is 0.11-0.20 seconds
For the height,measure the start of the P wave to start of QRS
Shape is prolonged and indicates a conduction block
Orientation: shortened indicates accelerated conduction or junctional in origin

QRS:
Ventricular depolarization 
0.06-0.11 seconds
The height to shape to orientation:
Q-first negative deflection
R- first positive deflection
S- negative deflection after R wave 

ST:
Represents the interval between the ventricular depolarization and repolarization
Duration to height: measure from end of QRS (J point) to beginning of T wave
Shape to orientation:
In relation to iso-electric line ;depression/negative indicates ischemia
Elevation or positive indicates injury

24
Q

On a normal ECG paper 1 small square is equal to what on the vertical and horizontal axis?
What about 1 large square? What about 2 large squares on vertical axis and 5 large squares on horizontal axis

A

Vertical: small square- 1mm (0.1mV)
Large square-5mm(0.5mV)
2 large squares-1mV

Horizontal: small square - 0.04 (40msec)
Large square-0.2(200msec )
5 large squares -1sec(1000msec)

25
Q

Where are the leads placed on the body

10 electrodes required to produce 12-lead ECG
What does aVL,aVF and aVR mean

A

V1 Fourth intercostal space to the right of the sternum.
V2 Fourth intercostal space to the left of the sternum.
V3 Directly between leads V2 and V4.
V4 Fifth intercostal space at midclavicular line.
V5 Level with V4 at left anterior axillary line.
V6 Level with V5 at the midaxillary line. (Directly under the midpoint of the armpit)
R - Right arm(RA)
L - Left arm
F - Left leg(LL)
N - Right leg

aVR means augmented Vector Right; the positive electrode is on the right shoulder. aVL means augmented Vector Left; the positive electrode is on the left shoulder. aVF means augmented Vector Foot; the positive electrode is on the foot.

26
Q

What five things do you check for in analyzing the ECG paper
How many big boxes is 60 seconds
How many boxes is 1 second
How do you measure the rate

A
Regularity
Rate
QRS
PR interval 
P waves 

5 large boxes is 1 second
300 large boxes is 60 seconds
Rate is 300/number of large boxes

27
Q

How do you manage sinus tachycardia and what’s the ecg pattern

A
Sinus tachycardia
•Look for the cause:
•Infection
•Autoimmune conditions
•Drugs
•Anxiety
•Don’t forget pulmonary embolism in at-risk patients

Treat the cause
•Usually that brings it down
•Slow it down
•Beta blockers

•Monitor

28
Q

What is DKA
Which patients does it usually occur in?

A

Diabetic Ketoacidosis (DKA) is an acute metabolic complication of Diabetes caused by
absolute or relative insulin deficiency.
• Commonly occurs in patients in type 1 diabetes
but also occurs is some patients with type 2
diabetes, often of Afro-Caribbean or Hispanic
organ. (Ketosis prone type 2 diabetes)

29
Q

How is DKA diagnosed

A

PATHOPHYSIOLOGY
• DKA is a complex disorder. Metabolic state is
characterized by;
1. Known DM or Hyperglycaemia (RBS >11.1mmol/L)
2. Ketonaemia (>3mmol
(< Ketonuria(>2+ on urine
dipstick
3.Acidosis (pH <7.2 or 7.3and/ or Bicarbonate < 15mmol/L

30
Q

How does DKA occur(Patho) and name three precipitants of DKA

A

Lack of insulin is accompanied by an increase in
counter-regulatory hormones.(glucagon,
cortisol, growth hormone and adrenaline)
• Increase in counter-regulatory hormones results
in enhanced hepatic gluconeogenesis and
glycogenolysis leading to hyperglycaemia

• Enhanced lipolysis increases free fatty acids
which are metabolized to ketones (acetone,
acetoacetate and 3- B hydroxy butyrate) and
causes a metabolic acidosis

Hyperglycemia leads to Glycosuria which leads to Osmotic diuresis (leads to loss of Loss of Na, Cl, Partial pressure of Oxygen, K
Ca, Mg, and N ) leading to Decreased GFR leading to Severe hyperglycemia leading to
Intracellular dehydration causing impaired consciousness or leading to Dehydration and
Hemoconcentration causing
Shock

Ketoacidosis leads to vomiting ,metabolic acidosis,compensatory tachypnea leading to dehydration and hemoconcentration then shock

Precipitants:
Infarction
Infection
Not taking meds properly

31
Q

State ten causes of DKA
State six ddx of DKA

A

IMPORTANT CAUSES OF DIABETIC KETOACIDOSIS
❖Omission or reduce daily insulin injection
❖Infection
❖Pregnancy
❖Hyperthyroidism
❖Substance abuse (cocaine)
❖Medication; steroids, thiazides, antipsychotics
❖Heat related illness
❖CVA
❖GI hemorrhage
❖Myocardial infection ❖Pulm0nary embolism ❖Pancreatitis
❖Major trauma
❖Surgery

Differential Diagnosis For Diabetic Ketoacidosis
• Alcoholic Ketoacidosis
• Starvation Ketoacidosis
• Renal Failure
• Lactic acidosis
• Salicylates
• Ethylene
• Methanol

32
Q

State three symptoms of DKA according to each system (neurological,CVS,Resp,GIT )

A

SIGNS AND SYMPTOMS(Clinical Features)
➢Hyperglycemia typically results in polyphagia,polyuria and polydipsia
➢Cardiovascular – hypotension and tachycardia due to dehydration
➢Gastrointestinal – abdominal pain, nausea and vomiting
➢Respiratory – kussmaul`s breathing (respiratory compensation for metabolic acidosis) and the smell of acetone on the breath
➢Neurological – AMS, confusion, coma

33
Q

State ten investigations for DKA

A

INVESTIGATION (DKA)
1. Blood Ketone Level
2. Glucose (bedside meter and confirmed with a laboratory venous plasma sample.
3. Venous blood gas – assess acid-base status
4. Blood tests – urea, electrolytes, FBC, Cl and bi
carbonate.
5. Infective screen – blood culture, urinalysis and
culture, Ch𝑒𝑠𝑡 𝑋𝑟𝑎𝑦.
6. ECG and Cardiac monitoring
7. Urinalysis
8. Serum osmolality (2*(Na + K) + urea + glucose

34
Q

State four signs of SEVERITY AND MARKERS OF POORER OUTCOME in a. Biochemical markers b.patient factors

A

SIGNS OF SEVERITY AND MARKERS OF POORER OUTCOME
Need for HDU\ICU level care
Biochemical Markers
✓Venous pH < 7.1
✓HC𝑂 < 5mmol\L
✓Blood ketones > 6mmol/L
✓Serum osmolality > 320mmol\L ✓Hypokalemia on admission (k<3.5)

SIGNS OF SEVERITY AND MARKERS OF POORER OUTCOME CONT. Patient Factors • Reduced level of consciousness • Hypotension • Hypoxia • Age > 65 years • Significant cardiac or Renal co—morbidity  • Newly diagnosed diabetes • Oliguria
35
Q

What is the goal of treatment in DKA

A

Goal of treatment
▪Correct volume deficit
▪Correct acid-base imbalance ▪Correct electrolyte abnormalities
▪Administer insulin
▪Treat the underlying causes

36
Q

How is DKA managed
Start from primary surveys and all

A

General Measures
• Ensure patency and maintenance of airway
• High flow oxygen should be given
• If he patient is unconscious advanced airway management and intubation will be required
• NG tube will be required if patient in vomiting or unconscious to prevent aspiration
• Two (2) IV cannulae

MANAGEMENT CONT. • Nil per mouth for at least 6hours (gastroparesis is common) • Urinary catheter • Broad-spectrum antibiotics if infection is suspected. • Consider LMWH eg, enoxaparin as prophylaxis against DVTs \PE

Fluid Replacement:
➢Use normal (0.9%) saline to replace the fluid deficit
➢Average fluids loss in DKA is 100ml\kg
➢If the glucose ≤ 14mmol/L, than 10% Dextrose
should be given at rate of 125ml\hr alongside the 0.9% sodium chloride
➢The insulin must not be stopped because it is required
to switch of ketone production.

Replace fluid if systolic bp is less than 90mmhg.
500ml 0.9% sodium (if sys BP <90mmhg) chloride over 10-15mins

-Repeat if necessary
• 0.9%sodiumchloride1Lover 1hr
• 0.9%sodiumchloride1Lwith KCl over 2hrs
• 0.9%sodiumchloride1Lwith KCl over 2hrs
sodiumchloride1Lwith KCl over 4hrs
• 0.9%sodiumchloride1Lwith KCl over 4hrs
• 0.9%sodium chloride1L with KCl over 6hrs

Insulin:
0.1iu/kg/hr

KCL infusion:
Deficit plus maintenance to correct Hypokalemia

Treat the precipitant of the DKA and infection if present

37
Q

What is the insulin regimen for DKA
When do you set up DNS in DKA or put patient on sliding scale

A

0.1iu/kg/hr (70iu in 50 mls RL or NS over 10 hours so 7iu every one hour) insulin and keep checking ketones till they clear and check sugars every hour and when it goes down to 13mmol/L then set up DNS. Or when it goes down to 13mmol/L it is likely ketones have cleared so you put patient on sliding scale

Insulin replacement
▪The only indication for delaying insulin is a serum K < 3.3mmo\L
▪Patients with initial serum K < 3.3mmo\L should receive fluid and K replacement prior to insulin
▪Fixed rate intravenous insulin infusion is now recommended rather than a sliding scale

The rate of insulin infusion is 0.1 unit\Kg\ hour (ie 7 units\hour if the patient weighs 70Kg).
For HHS, the rate of insulin infusion is 0.05iu/kg/hr
▪An initial bolus dose of insulin is no longer recommended.
▪The response to insulin infusion pump is reviewed after 1 hour.
▪If blood glucose is not dropping by 3-5mmol\hr and capillary ketone by 0.5mmol\hr, the rate of infusion is increased by 1U\hr.

MANAGEMENT CONT. • Monitor blood glucose, capillary ketones and urine output hourly • Urea and Electrolytes 4-hourly, Venous blood gas 0,2,4,8,12 • Monitor urinary ketones • The fixed rate insulin is continued until ; 1. Capillary ketones is < 0.3
      
MANAGEMENT CONT. 2. Venous pH > 7.3 3. Venous bicarbonate > 18 4. No urinary ketones (may take longer to clear) • At this point If patient is eating and drinking regularly, change to SC insulin regimen and stop IV insulin pump 1-2 ours afterwards

If patient is not eating and drinking, change to IV sliding scale.

38
Q

What is the KCL regimen for DKA

A

So if patient comes with Hypokalemia, correct K deficit and give maintenance potassium

Normokalemia- give maintenance KCl fluid

Hyperkalemia: don’t give potassium but use the BIG KDrop for management of hyperkalemia

Potassium replacement (KCL) ✓Potassium levels are often high on admission
✓Potassium levels however falls rapidly under the action of insulin
✓Regular potassium monitoring is mandatory

Suggested regimen for potassium. supplementation;    Plasma potassium (mmol\L):   a.If > 5.50mmol\L b.If. 3.5-5.5mmol\L c.If < 3.5

Amount of K(mmol) to add to each litre of fluid
a.Nil
b.Do 40mmol\L
c.Do 60-80mmol\L (HDU support required, seek specialist advise.

NB: Monitor urine output to ensure
> 30ml\hr

39
Q

When can a patient with DKA be converted to subcutaneous insulin?

A

Patients with DKA can be converted to an appropriate SC insulin regime when biochemically stable (blood ketone < 0.3 and pH> 7.3) and the patient is ready and able to eat.

40
Q

What is the DIFFERENCE IN MANAGEMENT BETWEEN ADULT AND PEDIATRIC DKA
How do you estimate th degree of dehydration

A

DIFFERENCE IN MANAGEMENT BETWEEN ADULT AND PEDIATRIC DKA
Fluid management in children with DKA
• Resuscitation fluids – if child is shocked (weak peripheral pulse, prolonged capillary refill, with tachycardia, and\or hypertension) they should receive bolus of 10ml\kg 0.9% sodium chloride. This can be repeated up to 3 times (30ml\kg)

• Rehydration fluid – is calculated based on the percentage dehydration multiplied by the body weight (kg) e.g, Deficit=%Dehydration×𝐵𝑜𝑑𝑦𝑤𝑒𝑖𝑔h𝑡 𝑘𝑔 The degree of dehydration can be estimated from the child`s clinical features.
       
• Maintenance fluids – The APLS formula.  The APLS maintenance fluid requirement ; Weight (kg) - ml\kg\24h First 10 kg - 100ml Second 10 kg – 50ml Subsequent kg – 20ml
      
Once shock has been treated fluids are calculated over a 48hr period using the following formula; 48 fluid requirement= Maintenance+ Rehydration- Resuscitation already given

Estimating the degree of dehydration:
Percentage dehydration
a.Mild, 3%

b.Moderate, 5%

c.Severe, 8%

d.Shocked

Clinical features
a.Only just clinically detectable
b.Dry mucous membranes, reduced skin turgor
c.As for moderate plus sunken eyes, poor capillary refill.

d.Severely ill with poor perfusion, thready rapid pulse

41
Q

State six complications of DKA

A

COMPLICATIONS OF DKA
• Hypokalaemia and hyperkalaemia • Hypoglycaemia
• Cerebral oedema
• Pulmonary oedema
• Aspiration pneumonia
• CVA
• MI
•Seizures due to acidosis leading to cerebral edema
Most DKA patients are dehydrated