Type 1 Diabetes

Basic Physiology

Eating carbohydrates causes in a rise in blood glucose (sugar) levels. As the body uses these carbohydrates for energy there is a fall in blood glucose levels. The body ideally wants to keep blood glucose concentration between 4.4. and 6.1 mmol/l.

Insulin is a hormone produced by the pancreas that reduces blood sugar levels. It is produced by the beta cells in the Islets of Langerhans in the pancreas. It is an anabolic hormone (a building hormone). It is always present in small amounts, but increases when blood sugar levels rise. Insulin reduces blood sugar in two ways: It causes cells in the body to absorb glucose from the blood and use it as fuel and it causes muscle and liver cells to absorb glucose from the blood and store it as glycogen. Insulin is essential in letting cells take glucose out of the blood and use it as fuel. Without insulin, cells cannot take up and use glucose.

Glucagon is a hormone also produced in the pancreas that increases blood sugar levels. It is produced by the alpha cells in the Islets of Langerhans in the pancreas. It is a catabolic hormone (a breakdown hormone). It is released in response to low blood sugar levels and stress. It tells the liver to break down stored glycogen into glucose. This process is called glycogenolysis. It also tells the liver to convert proteins and fats into glucose. This process is called gluconeogenesis.



Ketogenesis occurs when there is insufficient glucose supply and glycogens stores are exhausted, such as in prolonged fasting. The liver takes fatty acids and converts them to ketones. Ketones are water soluble fatty acids that can be used as fuel. They can cross the blood brain barrier and be used by the brain as fuel. Producing ketones is normal and not harmful in healthy patients when under fasting conditions or on very low carbohydrate, high fat diets. Ketones levels can be measured in the urine by “dip-stick” and in the blood using a ketone meter. People in ketosis have a characteristic acetone smell to their breath.

Ketone acids (ketones) are buffered in normal patients so the blood does not become acidotic. When underlying pathology (i.e. type 1 diabetes) causes extreme hyperglycaemic ketosis this results in a metabolic acidosis that is life threatening. This is called diabetic ketoacidosis.


Type 1 Diabetes

Type 1 diabetes mellitus (T1DM) is a disease where the pancreas stops being able to produce insulin. What causes the pancreas to stop producing insulin is unclear. There may be a genetic component. It may be triggered by certain viruses, such as the Coxsackie B virus and enterovirus. When there is no insulin being produced, the cells of the body cannot take glucose from the blood and use it for fuel. Therefore the cells think the body is being fasted and has no glucose supply. Meanwhile the level of glucose in the blood keeps rising, causing hyperglycaemia.


Pathophysiology of Diabetic Ketoacidosis (DKA)

Diabetic ketoacidosis occurs in type 1 diabetes where the person is not producing adequate insulin themselves and is not injecting adequate insulin to compensate for this. It occurs when they body does not have enough insulin to use and process glucose. The main problems are ketoacidosis, dehydration and potassium imbalance.


As the cells in the body have no fuel and think they are starving they initiate the process of ketogenesis so that they have a usable fuel. Over time the patient gets higher and higher glucose and ketones levels. Initially the kidneys produce bicarbonate to counteract the ketone acids in the blood and maintain a normal pH. Over time the ketone acids use up the bicarbonate and the blood starts to become acidic. This is called ketoacidosis.


Hyperglycaemia overwhelms the kidneys and glucose starts being filtered into the urine. The glucose in the urine draws water out with it in a process called osmotic diuresis. This causes the patient to urinate a lot (polyuria). This results in severe dehydration. The dehydration stimulates the thirst centre to tell the patient to drink lots of water. This excessive thirst is called polydipsia.

Potassium Imbalance

Insulin normally drives potassium into cells. Without insulin potassium is not added to and stored in cells. Serum potassium can be high or normal as the kidneys continue to balance blood potassium with the potassium excreted in the urine, however total body potassium is low because no potassium is stored in the cells. When treatment with insulin starts patients can develop severe hypokalaemia (low serum potassium) very quickly and this can lead to fatal arrhythmias.


Presentation of DKA

This is a life threatening medical emergency. The pathophysiology described above leads to:

  • Hyperglycaemia
  • Dehydration
  • Ketosis
  • Metabolic acidosis (with a low bicarbonate)
  • Potassium imbalance

The patient will therefore present with symptoms of these abnormalities:

  • Polyuria
  • Polydipsia
  • Nausea and vomiting
  • Acetone smell to their breath
  • Dehydration and subsequent hypotension
  • Altered Consciousness
  • They may have symptoms of an underlying trigger (i.e. sepsis)

The most dangerous aspects of DKA are dehydration, potassium imbalance and acidosis. These are what will kill the patient. Therefore the priority is fluid resuscitation to correct the dehydration, electrolyte disturbance and acidosis. This is followed by an insulin infusion to get the cells to start taking up and using glucose and stop producing ketones.


Diagnosing DKA

Check the local DKA diagnostic criteria for your hospital. To diagnose DKA you require:

  • Hyperglycaemia (i.e. blood glucose > 11 mmol/l)
  • Ketosis (i.e. blood ketones > 3 mmol/l)
  • Acidosis (i.e. pH < 7.3)


Treating DKA (FIG-PICK)

Follow local protocols carefully.

  • F – Fluids – IV fluid resuscitation with normal saline (e.g. 1 litre stat, then 4 litres with added potassium over the next 12 hours)
  • I – Insulin – Add an insulin infusion (e.g. Actrapid at 0.1 Unit/kg/hour)
  • G – Glucose – Closely monitor blood glucose and add a dextrose infusion if below a certain level (e.g. 14 mmol/l)
  • P – Potassium – Closely monitor serum potassium (e.g. 4 hourly) and correct as required
  • I – Infection – Treat underlying triggers such as infection
  • C – Chart fluid balance
  • K – Ketones – Monitor blood ketones (or bicarbonate if ketone monitoring is unavailable)

Establish the patient on their normal subcutaneous insulin regime prior to stopping the insulin and fluid infusion.

Remember as a general rule potassium should not be infused at a rate of more than 10 mmol per hour.


Long Term Management of Type 1 Diabetes

Patient education is essential. Monitoring and treatment is relatively complex. The condition is life-long and requires the patient to fully understand and engage with their condition. It involves the following components:

  • Subcutaneous insulin regimes
  • Monitoring dietary carbohydrate intake
  • Monitoring blood sugar levels on waking, at each meal and before bed
  • Monitoring for and managing complications, both short and long term

Insulin is usually prescribed as a combination of a background, long acting insulin given once a day and a short acting insulin injected 30 minutes before intake of carbohydrate (i.e. at meals). Insulin regimes are initiated by a diabetic specialist.

Injecting into the same spot can cause a condition called “lipodystrophy”, where the subcutaneous fat hardens and patients do not absorb insulin properly from further injections into this spot. For this reason patients should cycle their injection sites.


Short Term Complications

Short term complications relate to immediate insulin and blood glucose management.

  • Hypoglycaemia
  • Hyperglycaemia (and DKA)


Hypoglycaemia is a low blood sugar level. Most patients are aware of when they are hypoglycaemic by their symptoms, however some patients can be unaware until severely hypoglycaemic. Typical symptoms are tremor, sweating, irritability, dizziness and pallor. More severe hypoglycaemia will lead to reduced consciousness, coma and death unless treated.

Hypoglycaemia needs to be treated with a combination of rapid acting glucose such as lucozade and slower acting carbohydrates such as biscuits and toast for when the rapid acting glucose is used up. Options for treating severe hypoglycaemia are IV dextrose and intramuscular glucagon.


If the patient is hyperglycaemic but not in DKA then they may require their insulin dose to be increased. Patients will get to know their own individual response to insulin and be able to administer a dose to correct the hyperglycaemia. For example, they may learn that 1 unit of novorapid reduces their sugar level by around 4 mmol. Be conscious that it can take several hours to take effect and repeated doses could lead to hypoglycaemia.

If they meet the criteria for DKA then they need admission for treatment of DKA.


Long Term Complications

Chronic exposure to hyperglycaemia causes damage to the endothelial cells of blood vessels. This leads to leaky, malfunctioning vessels that are unable to regenerate. High levels of sugar in the blood also causes suppression of the immune system, and provides an optimal environment for infectious organisms to thrive.

Macrovascular Complications

  • Coronary artery disease is a major cause of death in diabetics
  • Peripheral ischaemia causes poor healing, ulcers and “diabetic foot
  • Stroke
  • Hypertension

Microvascular Complications

  • Peripheral neuropathy
  • Retinopathy
  • Kidney disease, particularly glomerulosclerosis

Infection Related Complications

  • Urinary Tract Infections
  • Pneumonia
  • Skin and soft tissue infections, particularly in the feet
  • Fungal infections, particularly oral and vaginal candidiasis




When we check HbA1c we are counting glycated haemoglobin, which is how much glucose is attached to the haemoglobin molecule. This is considered to reflect the average glucose level over the last 3 months because red blood cells have a lifespan of around 3-4 months. We measure it every 3 – 6 months to track progression of the patient’s diabetes and how effective the interventions are. It requires a blood sample sent to the lab, usually red top EDTA bottle.

Capillary Blood Glucose

This is measured using a little machine called a glucose meter that gives an immediate result. Patients with type 1 and type 2 diabetes rely on these machines for self-monitoring their sugar levels.

Flash Glucose Monitoring (e.g. FreeStyle Libre)

This uses a sensor on the skin that measures the glucose level of interstitial fluid. There is a lag of 5 minutes behind blood glucose. This sensor records the glucose readings at short intervals so you get a really good impression of what the glucose levels are doing over time. The user needs to use a “reader” to swipe over the sensor and it is the reader that shows the blood sugar readings. Sensors need replacing every 2 weeks for the FreeStyle Libre system. It is quite expensive and NHS funding is only available in certain areas at the time of writing. The 5 minute delay also means it is necessary to do capillary blood glucose checks if hypoglycaemia is suspected.


Last updated November 2018