History of previous anaesthesia
Certain conditions are particularly relevant to anaesthesia.
Intubation is difficult in about 1-3% of cases and impossible in about 0.05-0.3%. It is an important cause of morbidity and mortality, especially in emergency anaesthesia, and is not always predictable.
Anaphylactic or anaphylactoid reactions to anaesthetic drugs are commoner amongst members of the same families, and may be more serious in atopic individuals or in those sensitive to other drugs. A history of collapse after induction requiring cancellation and/or postoperative intensive care is suggestive.
This is a rare autosomal dominant condition triggered by inhalational anaesthetic vapours and probably suxametho-nium. There is a certain predisposition in muscular dystrophy, strabismus and cleft palate. Malignant hyperpyrexia presents with acute cardiorespiratory collapse manifested by cyanosis, hypercapnia, muscle rigidity, acidosis, tachyarrhythmias and a huge temperature rise. Pathologically, there is uncontrolled muscle contraction and energy consumption by the sarcoplasmic reticulum. Treatment is by cardiovascular support and administration of dantrolene. Survivors and screened relatives may carry a 'medical alert' warning and will usually be aware of the condition.
Suxamethonium, a depolarising muscle relaxant, is metabolised slower than normal due to a recessive abnormality of the plasma cholinesterase enzyme. There is delayed recovery in breathing effort after surgery, requiring prolongation of anaesthesia (to avoid awareness) and ventilation.
This is a group of inherited disorders in haem synthesis. Some anaesthetic agents such as barbiturates (thiopentone), in addition to alcohol and sulphonamides, may precipitate crisis of abdominal pain, cardiovascular instability or neuro-psychiatric manifestations.
This constitutes a group of autosomally inherited abnormalities in haemoglobin structure and function such that hypox-aemia triggers polymerisation of haemoglobin (Hb). This leads to a change in shape and a reduction in deformability of red cells which cause microvascular occlusion and haemolysis. Manifestations include haemolytic anaemia, susceptibility to infections, and ischaemic type pain and organ dysfunction, mostly in the lungs, spleen, vasculature and bone marrow. The genetic mutation is prevalent in sub-Saharan Africa, the Caribbean, parts of Asia and some parts of the south-eastern Mediterranean and the Arabian peninsula. It can be screened by an agglutination test and diagnosed by Hb electrophoresis.
A preoperative diagnosis is important, but should not delay life-saving surgery, when it is assumed that the at-risk patient has sickle cell disease. Anaesthesia during sickling crises has a high mortality and should be delayed.
The Hb electrophoresis distinguishes different Hb abnormalities and is the definitive diagnostic test. Sickle precipitation tests ('sickle dex', etc.) detect agglutination but cannot distinguish between the different variants (Tables 2.1 and 2.2).
Table 2.1. Sickle states.
Was this article helpful?