Acute Complications of Diabetes Flashcards by Emma Coakley

What does hypoglycaemia mean?

hypo = low
glyc = glucose
aemia = blood

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What is the clinical diagnosis of hypoglycaemia?

<4mmol/L

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How many people worldwide are estimated to be affected by hypoglycaemia?

460 million

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When a patients blood glucose drops <4mmol/L what systems combine to try and increase the bodies blood glucose levels?

autonomic

- sympathetic activity

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When a patients blood glucose drops <4mmol/L the autonomic system attempt to increase the bodies blood glucose levels through sympathetic stimulation. What 2 key hormones are released and which gland releases them?

adrenal gland (medulla) = adrenalin

- pancreas = glucagon

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What are the 3 most common signs that we as clinicians can see in a patient who is experiencing hypoglycaemia?

shaking/trembling
pallor
sweating

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3 of the most common signs that we as clinicians can see in a patient who is experiencing hypoglycaemia are:

1 - shaking/trembling
2 - pallor
3 - sweating

What are 7 other symptoms a patient may describe?

anxiety
tiredness
hunger
headaches
blurred vision
palpitations
lips/tongue tingling

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What does the term neuroglycopaenic mean?

low glucose supply to the brain

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Neuroglycopaenic refers to low blood glucose to the brain. What blood glucose level would we expect to see more neurological issues developing?

2.8mmol/L

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Neuroglycopaenic refers to low blood glucose to the brain, which is when blood glucose drops below 2.8mmol/L. What are some of the most common later signs of hypoglycaemia?

slurred speech
sower reactions
disorientation
seizures/fitting
coma
low concentration
dizziness
confusion
aggression or irritable

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What is Hypoglycaemia Unawareness?

patient is unaware that their blood glucose is dangerously low
Neuroglycopenia symptoms occur before autonomic symptoms

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Hypoglycaemia Unawareness is when a patient is unaware that their blood glucose is dangerously low and then neuroglycopenia symptoms occur before autonomic symptoms. What % of patients with T1DM experience this?

aprox 40%

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Hypoglycaemia Unawareness is when a patient is unaware that their blood glucose is dangerously low and then neuroglycopenia symptoms occur before autonomic symptoms, which occurs in aprox 40% of T1DM patients. What 3 things must have happened for this to occur?

sympathetic activity is reduced due to cellular adaptation to hypoglycaemia
leads to hypoglycaemia-associated autonomic failure
chronically low glucose in liver and glucagon in pancreas

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What are some of the most common causes that cause hypoglycaemia in patients?

increased/decreased carbohydrate intake (alcohol)
too much exercise
mismanaged medication (insulin, GLP-1)
alcohol
age and duration of diabetes
hypoglycaemia unawareness
impaired renal function
pregnancy/breast feeding

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How can excessive alcohol cause hypoglycaemia?

alcohol contains a lot of sugar which causes the body to produce excessive insulin
if food is not consumed alongside patients will have too much insulin and blood glucose drops

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If a patients has been identified as being hypoglycaemia (<4mmol/L), what would the immediate treatment be if the patient is conscious and able to swallow?

give 20g quick/rapid acting carbohydrates

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If a patients has been identified as being hypoglycaemia (<4mmol/L), the immediate treatment be if the patient is conscious and able to swallow, we would give the patient 20g of quick/rapid acting carbohydrates. How would we assess if the patients blood glucose has risen above 4mmol/L and if it has not what would we do next?

perform capillary blood glucose (CBG) after 10-15 minutes

- if still <4mmol/L give the patient an additional 20g of quick/rapid acting carbohydrates

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If a patients has been identified as being hypoglycaemia (<4mmol/L), the immediate treatment be if the patient is conscious and able to swallow, we would give the patient 20g of quick/rapid acting carbohydrates. We would then take a capillary blood glucose (CBG) after 10-15 minutes to assess if the blood glucose has risen >4mmol/L. If still <4mmol/L give the patient an additional 20g of quick/rapid acting carbohydrates. If you assess the CBG again after 10-15 minutes and the patients blood glucose is still <4mmol/L, what would then next immediate treatment option be?

hospital = intravenous dextrose (essentially a simple sugar)
home = glucagon injection administered

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Once we are happy that a patient is no longer hypoglycaemic (>4mmol/L), how would we treat the patient?

provide slow releasing carbohydrates

- 10-20 grams (food such as toast, biscuits)

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What are a few simple examples of 20g of fast acting carbohydrates?

200 ml pure fruit juice e.g. orange
120ml of original Lucozade®
6-7 Dextrosol® tablets (or 5 Glucotabs®)
3 – 4 Jelly babies
200mls coke
Glucojuice is equivalent of 15g of carbs

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If a diabetic patient is suspected of being hypoglycaemia and unconscious at home, what would a family/friend need to do?

call 999 and ask for help as this is a medical emergency

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If a diabetic patient is suspected of being hypoglycaemia and unconscious at home, and has been brought into hospital, what 2 things must we check?

ABCs
Airway, Breathing and Circulation
temperature (patients may become hypothermic)

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If a diabetic patient is suspected of being hypoglycaemia and unconscious at home, and has been brought into hospital, and we have checked their ABCs, what would be really important to measure to assess their consciousness?

glasgow coma scale (GCS)

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If a diabetic patient is suspected of being hypoglycaemia and unconscious at home, and has been brought into hospital, we have checked their ABCs, assessed their consciousness using the Glasgow Coma Scale, what do we need to do to assess if they are actually hypoglycaemia?

assess blood glucose

- check to see if <4mmol/L

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If a diabetic patient is suspected of being hypoglycaemia and unconscious at home, and is in hospital, what would we want to do with insulin and dextrose?

- insulin = if patient is taking insulin this would be stopped immediately - dextrose = patient would receive intravenous dextrose to raise blood glucose

If a patient is at home, is unconscious, unable to swallow and confirmed to being hypoglycaemic, what can a family/friend or on site clinical team member do?

- administer subcutaneous or intramuscular injection of glucagon

If a patient is at home, is unconscious, unable to swallow and confirmed to being hypoglycaemic, what can a family/friend or on site clinical team member do?

- administer subcutaneous or intramuscular injection of glucagon

If a patient is at home, is unconscious, unable to swallow and confirmed to being hypoglycaemic, and a family/friend or on site clinical team member has administered subcutaneous or intramuscular injection of glucagon, what should the normal response in blood glucose be within 10 minutes?

- 3.5-5.7 mmol/L

If a patient is at home, is unconscious, unable to swallow and confirmed to being hypoglycaemic, a family/friend or on site clinical team member can administered subcutaneous or intramuscular injection of glucagon. Which 3 groups of patients might be less responsive to glucagon injections?

- chronically malnourished - depleted glycogen stores - severe liver disease (low glycogen stores and/or metabolism)

If a patient is at home and has become hypoglycaemic and been administered with a glucagon injection and their blood glucose has risen to within 3.5-5.7 mmol/L, what must they then do?

- administer slow acting carbohydrates | - patient must be able to swallow safely

Dextrose is provided to patient intravenously when patients are hypoglycaemic. What is the recommended dose for a patient who is hypoglycaemic and requires dextrose administration?

- 20% dextrose - given in 100ml over 10-15 minutes - once recovered (4 hours), provide with 20g of slow acting carbohydrates

Dextrose is provided to patient intravenously when patients are hypoglycaemic. The recommended dose for a patient who is hypoglycaemic and requires dextrose administration is as follows: - 20% dextrose - given in 100ml over 10-15 minutes - once recovered (4 hours), provide with 20g of slow acting carbohydrates Why can it be dangerous to administer 50% dextrose?

- 50% is hypertonic and may cause the following: 1 - phlebitis (skin irritation) 2 - thrombosis (blood clot) at injection site 3 - overcorrection and hyperglycaemia

Dextrose is provided to patient intravenously when patients are hypoglycaemic. Insulin is normally stopped to allow blood glucose to rise following the administration of dextrose. However, when would we never stop insulin administration?

- in T1DM patient

What is diabetic ketoacidosis?

- excessive levels of ketone bodies in the blood - ketones are produced when glycogen/glucose levels are low - can donate their protons in blood, causing metabolic acidosis

When does diabetic ketoacidosis occur?

- pancreas secretes glucagon causing in response to low blood glucose - blood glucose levels are high but insulin is low or none at all - blood glucose cannot be absorbed as lack of insulin, can cause polyuria - body produces ketones from fatty acids for energy, but too much is acidic and dangerous

What is the incidence of does diabetic ketoacidosis occur in 10,000 of the diabetic population?

- 46-80

The incidence of diabetic ketoacidosis that occurs in 10,000 of the diabetic population is 46-80. What is the mortality rate?

- 4-10%

Which group of diabetic patients does 20% of diabetic ketoacidosis occur in?

- those with new onset diabetes

What is the diagnosis of diabetic ketoacidosis based on blood glucose?

- hyperglycaemia | - >11mmol/L

What are the 2 diagnostic criteria of diabetic ketoacidosis based on ketonaemia?

1 - capillary ketones >3 (hydrooxybuteric acid, most common one) 2 - urine ketones >2+

What is the 2 diagnostic criteria of diabetic ketoacidosis based on acidosis?

1 - serum bicard <15mmol/L | 2 - pH <7.3

In diabetic ketoacidosis why is it important to be aware of euglycaemic?

- normal blood glucose is present | - BUT ketonaemia and acidosis are present

The pathophysiology of ketoacidosis is complex and includes a number of factors which are based around insulin deficiency. What 2 things occur in adipose tissue?

- increased lipolysis (fatty acid breakdown fro triglycerides) and free fatty acids in the blood - decreased adipogensis (adipocyte differentiation, more fat cells essentially)

The pathophysiology of ketoacidosis is complex and includes a number of factors which are based around insulin deficiency. What 2 things occur in the liver?

- increased gluconeogenesis (non carb substrates into glucose) - decreased glycogenolysis (glucose stored as glycogen, normally the job of glucose)

The pathophysiology of ketoacidosis is complex and includes a number of factors which are based around insulin deficiency. What 2 things occur in the skeletal muscle?

1 - decreased glycogenolysis (glucose stored as glycogen, normally the job of glucose) 2 - decreased protein synthesis

The pathophysiology of ketoacidosis is complex and includes a number of factors which are based around insulin deficiency. What 4 hormones are secreted in an attempt to correct the problem?

1 - cortisol (increases gluconeogenesis in an attempt to increase blood glucose) 2 - growth hormone (opposite affect of insulin, so more glucose in blood) 3 - catecholamines (signal increase release of glucagon) 4 - glucagon (increase glucose release into blood)

Insulin deficiency can cause hyperglycaemia. What effect does this have on the concentration of solutes in the blood and what is this called?

- hyper-osmolarity due to high glucose concentration

Insulin deficiency causes hyperglycaemia, which in turn can lead to increased glucose to be present in the urine, what is this called?

- glycosuria

Insulin deficiency causes hyperglycaemia, which in turn can lead to increased glucose to be present in the urine, called glycosuria. This can then lead to 2 major effects on the patient, both linked with 2 much fluid leaving the body as urine. What are these 2 effects?

1 - dehydration | 2 - electrolyte loss

Insulin deficiency causes hyperglycaemia, which in turn can lead to increased glucose to be present in the urine, called glycosuria. This can then lead to dehydration and electrolyte loss. How does hyperglycaemia cause electrolyte loss?

- hyperglycaemia draw fluid from intra to extracellular space to dilute blood glucose - movement of H2O from intra to extracellular space causes hyponatraemia - the body therefore has too much extracellular fluid and attempt to remove it via diuresis - diuresis means glucose and electrolytes will be loss in the urine in an attempt to reduce blood volume and hyperglycaemia

Insulin deficiency causes hyperglycaemia, which in turn can lead to increased glucose to be present in the urine, called glycosuria, which can then lead to dehydration and electrolyte loss. Long term what effect can this have on renal function?

- damage to renal tubules | - impaired renal function or even failure

The effects of insulin deficiency and hyperglycaemia can have a number of detrimental effects, culminating in diabetic ketoacidosis. Ultimately, what is the life threatening event this will cause if left untreated?

- cardiovascular collapse | - most diabetic patients die of heart complications

What are the most common signs of diabetic ketoacidosis?

- polyuria - abnormal thirst (polydipsia) - nausea - abdominal pain - ketone breath (acetate causes pear drop sweets or nail varnish) - Kussmaul breathing (deep and laboured to remove CO2 and lower pH) - lethargy - confusion - coma

What are the 3 main ketone bodies that cause diabetic ketoacidosis?

1 - acetoacetate 2 - β-hydroxybutyrate 3 - acetatone

The 3 main ketone bodies that cause diabetic ketoacidosis are 1 - acetoacetate 2 - β-hydroxybutyrate 3 - acetatone No enzyme is required for the conversion of acetoacetate to acetone, but what enzyme is responsible for the conversion of acetoacetate to β-hydroxybutyrate?

- D-beta-hydroxybutyrate dehydrogenase

When trying to measure if a patient has diabetic ketoacidosis, what is the main ketone measured in clinical practice?

- acetoacetate | - BUT β-hydroxybutyrate is a better marker and kits are becoming available

What are some common precipitating factors that can cause diabetic ketoacidosis?

- infection - missed insulin doses - surgery - medications – steroids - alcohol (excessive sugar causes hyperglycaemia) and other illicit drugs - pregnancy and menstruation - serious illness – e.g. Myocardial Infarction - idiopathic

In a patient with diabetic ketoacidosis (DKA) there are multiple aspects that need to be addressed. One aspect is to address low K+ concentrations. There are 2 mechanisms explaining why K+ concentrations increase in DKA, initially causing hyperkalaemia, what are these 2 mechanisms?

- cells posses a H+ (enter the cell) / K+ (leave the cell) cation exchanger - DKA causes high ketone bodies causing increased H+ osmolality in plasma - 1st mechanism = H+ moves down concentration gradient into cells and K+ leaves the cell - 2nd mechanism = insulin activates Na+/K+ pump, no insulin means K+ cannot enter the cell ULTIMATELY CAUSES HYPOKALAEMIA AS K+ LOST IN THE URINE

In a patient with diabetic ketoacidosis (DKA), initially hyperkalaemia occurs as K+ leaves the cell in exchange for H+. The excessive K+ in the blood (hyperkalaemia) is then excreted in urine, resulting hypokalaemia. This process is due to 2 mechanisms: - 1st mechanism = H+ moves down concentration gradient into cells and K+ leaves the cell - 2nd mechanism = insulin activates Na+/K+ pump, no insulin means K+ cannot enter the cell How can K+ levels in DKA be addressed?

- return electrolyte balance between intra and extracellular space - address K+ depletion

In a patient with diabetic ketoacidosis (DKA), initially hyperkalaemia occurs as K+ leaves the cell in exchange for H+. The excessive K+ in the blood (initially hyperkalaemia) is then excreted in urine, resulting hypokalaemia. This process is due to 2 mechanisms: - 1st mechanism = H+ moves down concentration gradient into cells and K+ leaves the cell - 2nd mechanism = insulin activates Na+/K+ pump, no insulin means K+ cannot enter the cell In addition to addressing the K+ depletion, what can DKA do to the breathing and why?

- respiratory compensation in form of hyperventilation to remove excessive CO2 - CO2 + H2O = H2CO3 (carbonic anhydrase) = H+ + HCO3- - purpose is to remove excessive H+

In a patient with diabetic ketoacidosis (DKA), initially hyperkalaemia occurs as K+ leaves the cell in exchange for H+. The excessive K+ in the blood (initially hyperkalaemia) is then excreted in urine, resulting hypokalaemia. Treating DKA needs to address hypokalaemia and excessive H+ (normally through breathing). What one other major thing needs to be addressed?

- dehydration

Based on the glasgow coma scale, what would be classed as severe diabetic ketoacidosis?

- <12 GCS

Based on the blood pH and bicarb levels, what would be classed as severe diabetic ketoacidosis?

- pH = <7.1 | - bicarb = <5

In a patient with severe diabetic ketoacidosis, what 3 things may be a sign of shock?

- low BP (due to polyuria) - organ failure (kidney disease) - low potassium

When managing a patient with diabetic ketoacidosis what are the first 3 things we must assess?

- airways - breathing - circulation

When managing a patient with diabetic ketoacidosis (DKA), why would we need to do a blood culture?

- infection is a precipitating cause of DKA | - administer broad spectrum antibodies if infection

When managing a patient with diabetic ketoacidosis (DKA), what will be administered through a cannula and what would we measure to assess the effectiveness of this?

- fluid administered via cannula (based on urine output and BP) - assess venous blood gas whilst administering fluids and check K+

When managing a patient with diabetic ketoacidosis (DKA), one fluid will help address fluid levels and electrolytes. What would be administered through a second cannula?

- insulin based on patients weight

The aim of management in a patient with diabetic ketoacidosis is reduce ketones, or decrease bicarbonate and/or blood glucose, K+ levels. What are the levels that we would want each of the following to reduce by: - ketones - bicarbonate - glucose - potassium

- ketones = reduction of 0.5mmol/l/h - bicarbonate = increase of 3mmol/L/h - glucose= reduction of 3mmol/L/h = potassium = maintain normal range

In a patient with diabetic ketoacidosis they will be administered with insulin to reduce the hyperglycaemia. in addition to insulin, what else is administered alongside and when would it be administered?

- dextrose to avoid hypoglycaemia at 10% with blood glucose <14mmol/L - administer at 125ml/hour NO K+ ADDED AT THIS STAGE

Using the standard treatment approach for diabetic ketoacidosis, how long should it take for ketonaemia and acidosis to be corrected?

- within 24 hours

In a patient with diabetic ketoacidosis, what 4 common complications can affect the treatment?

1 - cerebral oedema 2 - hypo/hyperkaelaemia 3 - hypoglycaemia 4 - pulmonary oedema (due to fluid administration)

What is a Hyperosmolar Hyperglycaemia State (HHS)?

- a state where the blood glucose is high in blood - results in hyperosmolality state - generally associated with low or no insulin

A Hyperosmolar Hyperglycaemia State (HHS) is where the blood glucose is high in blood, resulting in a hyperosmolality state, generally associated with low or no insulin. How common is HHS in hospitalised patients and what is the associated mortality of HSS?

- <1% of patients with diabetes | - 10-20% mortality

In a patient with Hyperosmolar Hyperglycaemia State (HHS) what is the pathway for shock and cardiovascular failure?

- patient presents with HSS so hyperglycaemia and hyperosmolality state - glycosuria occurs follow by loss of electrolytes (Na+, K+ and phosphates) - dehydration occurs due to loss of fluids - renal failure occurs - shock and cardiovascular failure

A Hyperosmolar Hyperglycaemia State (HHS) is where the blood glucose is high in blood, resulting in a hyperosmolality state, generally associated with low or no insulin. Does lipolysis occur in HSS?

- no

A Hyperosmolar Hyperglycaemia State (HHS) is where the blood glucose is high in blood, resulting in a hyperosmolality state, generally associated with low or no insulin. What are the 4 diagnostic criteria for HSS?

- hypovolaemia - hyperglycaemia >30 mmol/L (no significant hyperketonaemia (DKA) (7.3, bicarbonate >15 mmol/L) - osmolality >320 mosmol/kg

How do we calculate osmolality and what is the normal range?

- (2x (Na+ mmol/L + K+ mmol/L) + (urea mmol/L) + glucose (mmol/l) - normal values range from 275 to 295 mmol/kg

- insidious onset (slow gradual onset) - polyuria - polydipsia (excessive thirst) - muscle weakness - blurred vision - hallucinations - coma - clinical signs of dehydration

- infection - myocardial infarction - high dose steroid therapy - cocaine

A Hyperosmolar Hyperglycaemia State (HHS) is where the blood glucose is high in blood, resulting in a hyperosmolality state, generally associated with low or no insulin. How is HHS treated?

- replace fluid loss - correct electrolytes and osmolality (measure frequently) - reduce glucose - treat underlying precipitant - prevent complications

A Hyperosmolar Hyperglycaemia State (HHS) is where the blood glucose is high in blood, resulting in a hyperosmolality state, generally associated with low or no insulin. Not always given, but when would a low dose of insulin be administered in treating HSS?

- glucose not reducing sufficiently (5mmol/L/h) | - if ketones are present

At normal level the ratio of acetoacetate to β-hydroxybutyrate is 1:1. However, during diabetic ketoacidosis, what does this ratio reach?

- acetoacetate to β-hydroxybutyrate is 1:10

Acute Complications of Diabetes Flashcards

(83 cards)