Emergencies - Anaphylactic shock Flashcards
Describe anaphylaxis
Anaphylaxis is a life-threatening medical emergency.
It is caused by a severe type 1 hypersensitivity reaction. Immunoglobulin E (IgE) stimulates mast cells to rapidly release histamine and other pro-inflammatory chemicals. This is called mast cell degranulation.
This causes a rapid onset of symptoms, with airway, breathing and/or circulation compromise.
What is a key feature that differentiates between anaphylaxis and non-anaphylactic allergic reactions?
Compromise of the airway, breathing or circulation
Presentation of anaphalaxis
Patients present with a history of exposure to an allergen (although it can be idiopathic). There will be rapid onset of allergic symptoms:
- Urticaria
- Itching
- Angio-oedema, with swelling around lips and eyes
- Abdominal pain
Additional symptoms that indicate anaphylaxis are:
- Shortness of breath
- Wheeze
- Swelling of the larynx, causing stridor
- Tachycardia
- Lightheadedness
- Collapse
Initial assessment of acutely unwell child is with an ABCDE approach, assessing and treating:
A – Airway: Secure the airway
B – Breathing: Provide oxygen if required. Salbutamol can help with wheezing.
C – Circulation: Provide an IV bolus of fluids
D – Disability: Lie the patient flat to improve cerebral perfusion
E – Exposure: Look for flushing, urticaria and angio-oedema
Once a diagnosis of anaphylaxis is established, there are three medications given to treat the reaction:
Intramuscular adrenalin, repeated after 5 minutes if required
Antihistamines, such as oral chlorphenamine or cetirizine
Steroids, usually intravenous hydrocortisone
How should anaphylaxis be managed after the acute event?
Children should be admitted to the paediatric unit for observation as biphasic reactions can occur, meaning they can have a second anaphylactic reaction after successful treatment of the first.
Anaphylaxis can be confirmed by measuring the serum mast cell tryptase within 6 hours of the event.
What are the main problems in diabetic ketoacidosis?
Ketoacidosis, dehydration and potassium imbalance
Pathophysiology of ketoacidosis in DKA
When the cells in the body have no fuel and think they are starving, they initiate the process of ketogenesis so they have a usable fuel. Over time the glucose and ketone levels get higher and higher. Initially the kidneys produce bicarbonate to buffer 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.
Pathophysiology of dehydration in DKA
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 polyuria and results in severe dehydration. The dehydration stimulates the thirst centre and leads to polydipsia.
Pathophysiology of potassium imbalance in DKA
Insulin normally drives potassium into cells. Without insulin, potassium is not added to and stored in cells. Serum potassium can be high or normal in diabetic ketoacidosis, however total body potassium is low because no potassium is stored in the cells. When treatment with insulin starts, patients can develop severe hypokalaemia very quickly and this can lead to fatal arrhythmias.
Why are children with DKA at high risk of developing cerebral oedema?
Dehydration and hyperglycaemia cause water to move from the intracellular space in the brain to the extracellular space. This causes the brain cells to shrink and become dehydrated. Rapid correction of dehydration and hyperglycaemia (with fluids and insulin) causes a rapid shift in water from the extracellular space to the intracellular space in the brain cells. This causes the brain to swell and become oedematous, which can lead to brain cell destruction and death.
Children being treated for DKA must be monitored closely for signs of cerebral oedema. What signs are looked for?
- Headaches
- Altered behaviour
- Bradycardia
- Change to conciousness
Presentation of DKA
- Polyuria
- Polydipsia
- Nausea and vomiting
- Weight loss
- Acetone smell to their breath
- Kausmaul breathing
- Dehydration and subsequent hypotension
- Altered consciousness
- Symptoms of an underlying trigger (i.e. sepsis)
What investigations would be required to diagnose DKA?
- Hyperglycaemia (i.e. blood glucose > 11 mmol/l)
- Ketosis (i.e. blood ketones > 3 mmol/l)
- Acidosis (i.e. pH < 7.3)
What are the two pillars of correcting DKA?
- Correct dehydration evenly over 48 hours. This will correct the dehydration and dilute the hyperglycaemia and the ketones. Correcting it faster increases the risk of cerebral oedema.
- Give a fixed rate insulin infusion. This allows cells to start using glucose again. This in turn switches off the production of ketones.
