H
H2 receptor antagonists. Competitive antagonists of H2 histamine receptors. Used to reduce histamine-mediated gastric acid secretion in: peptic ulcer disease; gastro-oesophageal reflux; those at risk of aspiration of gastric contents; and to reduce gastric/duodenal bleeding in patients in ICU. Their use in critically ill patients receiving enteral feeding is declining because they increase the risk of nosocomial chest infections. Have also been used with antihistamine drugs to reduce the severity of adverse drug reactions and other allergic responses involving histamine.
cimetidine: introduced first. Cheapest, but with more side effects. Inhibits hepatic microsomal enzymes.
ranitidine: fewer side effects than cimetidine and does not cause hepatic enzyme inhibition. Longer duration of action.
nizatidine: similar to ranitidine.
Marik PE, Vasu T, Hirani A, Pachinburavan M (2010). Crit Care Med; 38: 2222–8
Haemaccel, see Gelatin solutions
Haematocrit (Hct). Total red cell volume as a proportion of blood volume. Slightly higher in venous than arterial blood because of entry of chloride ions (chloride shift) into red cells with accompanying water entry. An easily measured index of O2-carrying capacity of the blood, assuming normal red cell haemoglobin concentration and function. Normal values: 0.4–0.54 (male); 0.37–0.47 (female). Haemodilution to a Hct of 0.3–0.35 may be beneficial for tissue O2 delivery (e.g. in critically ill patients) because of reduced blood viscosity and increased flow; a value below this level is thought to compromise O2 delivery.
Haemoconcentration. Increase in haematocrit and haemoglobin concentration following dehydration or plasma loss. Degree of haemoconcentration may indicate the extent of fluid deficiency. Does not occur immediately after haemorrhage, since red cells and plasma are lost together; compensatory mechanisms restoring blood volume cause subsequent haemodilution. In prolonged severe ‘irreversible’ shock, however, fluid shifts into the interstitium with resulting haemoconcentration.
Haemodiafiltration. Modification of continuous arteriovenous or venovenous haemofiltration (CAVHD or CVVHD respectively) in order to improve efficiency and solute clearance rate. Circuitry and other aspects are identical to those for haemofiltration except that 1–2 l/h of dialysate fluid is allowed to run counter-current to the blood flow on the filtrate side of the haemofilter (Fig. 79). Solute is cleared by a combination of diffusion and convection.
Haemodialysis. Dialytic technique for removal of solutes and water from blood by their passage across a semipermeable membrane into dialysis fluid (dialysate). Indications include renal failure, fluid overload and pulmonary oedema, electrolyte disturbances, severe acidosis and some cases of drug poisoning and overdoses.
vascular access: usually via a: ‘single needle’ single-lumen catheter (through which blood is withdrawn into the dialyser and then returned to the patient in an alternating cycle); double-lumen central venous catheter (or two single ones); Silastic arteriovenous shunt connecting adjacent vessels, e.g. radial artery/cephalic vein (Scribner shunt); or permanent arteriovenous fistula (see Shunt procedures).
passage of blood via an extracorporeal circuit to a semipermeable cellophane membrane or hollow fibre system. Traditional cellulose-based membranes may be associated with complement activation and subsequent inflammatory cascade; thus newer synthetic membranes (e.g. polyacrylonitrile, polysulphone) are increasingly used, although more expensive. Dialysate may be passed on the other side of the membrane, usually in a counter-current fashion. Blood flow is usually 150–300 ml/min. The following are exchanged:
– solutes: pass by diffusion from blood to dialysate, depending on the concentration gradient, size (mw) of solute, membrane porosity and duration of dialysis. Thus fluids of different composition may be used to remove different amounts of solute as required. Most dialysis fluids contain sodium, chloride, calcium, magnesium, acetate or bicarbonate (as an alkali source; bicarbonate itself cannot be added directly since it may precipitate calcium and magnesium) and variable amounts of glucose and potassium. Solutes may also pass across the membrane by applying a hydrostatic pressure across the membrane, thereby removing water (ultrafiltration); solutes that can pass through the membrane pores are swept along with the water (solvent drag).
anticoagulation of the extracorporeal circuit is required, e.g. with heparin or prostacyclin infused into the line upstream to the dialysis machine. Control of coagulation with infusion of protamine to the downstream line has been used but may be difficult.
Performed intermittently, e.g. for 4–6 h daily/weekly as required.
technical, e.g. related to vascular access and bleeding, air embolism, clotting within the circuit. Modern machines usually incorporate alarms and monitors for air bubbles.
hypotension: may be related to hypovolaemia, disequilibrium syndrome or acetate in the dialysate (thought to cause vasodilatation and cardiac depression; replacement with bicarbonate has been suggested, although it is more complex to achieve).
hypoxaemia: mechanism is unclear.
[Belding H Scribner (1921–2003), Seattle nephrologist]
Haemodilution. Lowering of haematocrit and haemoglobin concentration due to fluid shift, retention or administration. May follow compensatory restoration of blood volume after haemorrhage, or iv fluid therapy with only partial replacement of red cell losses. Also occurs as a physiological process in pregnancy. Reduction of haematocrit lowers blood viscosity and increases blood flow, although O2 content falls. Optimal haematocrit following acute blood loss is thought to be about 0.3; in addition to improved tissue blood flow, hazards of blood transfusion and risk of DVT are reduced. Animal studies of cerebral ischaemia have suggested reduced infarct size if early haemodilution is achieved, although human evidence is lacking.
Haemofiltration. Common form of renal replacement therapy used in the ICU. First described in 1977; its main benefit over haemodialysis is cardiovascular stability. Initially described as continuous arteriovenous haemofiltration (CAVH; Fig. 79a) using an extracorporeal circuit via a surgically performed arteriovenous shunt (see Shunt procedures) or using large-bore arterial and venous cannulae. Blood flow through the circuit relies upon the arterial–venous pressure difference.
Now more frequently employs a continuous veno-venous circuit (CVVH; Fig. 79b) using a large-bore double-lumen venous cannula and a peristaltic roller pump that incorporates monitors to detect air embolism and extremes of circuit pressure. Blood is pumped at 100–200 ml/min. Anticoagulation of the extracorporeal circuit, but not the patient, is achieved using heparin (200–1000 U/h) or prostacyclin (2–10 ng/kg/min). Anticoagulation is not usually necessary if the patient has a coagulopathy.
Both CAVH and CVVH rely on the passage of blood through a filter containing a highly permeable membrane (polysulphone, polyamide or polyacrylonitrile; surface area 0.6–1.0 m2) that acts as an artificial glomerulus. Ultrafiltration occurs by virtue of the hydrostatic pressure gradient between the blood and ultrafiltrate sides of filter; solute removal occurs because of convection. Water and solutes lost from the plasma are replaced by haemofiltration fluid containing water and electrolytes. Ultrafiltration can be slow and titrated to the patient response. Replacement fluid is infused into the ‘arterial’ limb of the circuit (pre-dilution) or, more usually, into the ‘venous’ limb after the filter (post-dilution). Pre-dilution may be useful when there is a high filtrate removal rate (> 10 l/day) or a high haematocrit (> 35%) as it decreases viscosity and subsequent clotting in the circuit. However, pre-dilution decreases the efficiency of the system as the blood being filtered contains a lower concentration of waste products.
Both CAVH and CVVH require an exchange of 12–20 l/day to achieve adequate solute clearance. Filtration can be increased by applying a negative pressure to the filtrate side of the filter or by increasing the distance between the filter and filtrate collecting chamber. In haemodiafiltration, dialysate fluid is passed through the filter to improve efficiency and solute clearance rate (Fig. 79c and 79d).
Complications are related to the extracorporeal circuit and vascular access (air embolism, clotting, haemorrhage, complement activation, infection), ultrafiltration (hypovolaemia), electrolyte loss (hyponatraemia, hypocalcaemia), hypothermia, metabolic alkalosis (use of large volumes of lactate-rich replacement fluid) and removal of therapeutic drugs, including parenteral nutrition.
It has been suggested that CAVH and CVVH have a beneficial effect in sepsis by removing pro-inflammatory cytokines, although this is controversial.
Haemoglobin (Hb). Red-coloured pigment in erythrocytes, composed of:
– Hb A (adult): two α chains, two β chains.
– Hb A2 (usually 2–3%): two α chains, two δ chains.
– Hb F (fetal): two α chains, two γ chains.
There are 141 amino acid residues in α chains; 146 in β, δ and γ chains.
Fetal Hb is normally replaced by Hb A within 6 months of birth, unless polypeptide chain production is abnormal, e.g.:
– thalassaemia: reduced synthesis of normal chains.
– haemoglobinopathies, e.g. sickle cell anaemia: abnormal β chains are synthesised.
haem: porphyrin derivative containing iron in the ferrous (Fe2+) state. One haem moiety, containing one iron atom, is conjugated to each polypeptide. Oxidation of the iron to the ferric (Fe3+) state forms methaemoglobin (high levels of which cause methaemoglobinaemia).
the iron atom in each haem moiety, remaining in the ferrous state but sharing one of its electrons, can reversibly bind one O2 molecule, forming oxyhaemoglobin. Thus each Hb molecule can bind four O2 molecules. In its deoxygenated form, the Hb molecule exists in a ‘taut’ configuration. Binding of one O2 molecule breaks salt linkages between α- and β-globin chains and produces a more ‘relaxed’ configuration. This results in increased affinity for further binding (cooperativity), resulting in the sigmoid-shaped oxyhaemoglobin dissociation curve. Affinity is reduced by increasing PCO2 (Bohr effect), acidity, temperature and amount of 2,3-DPG present. Fetal Hb has greater affinity for O2 than has adult Hb.
CO2 may bind reversibly to amino groups of the polypeptide chains, forming carbamino compounds (RNH2 + CO2 → RNHCO2H). Deoxygenated Hb has a greater affinity for CO2 than oxygenated (Haldane effect).
imidazole groups of histidine residues act as buffers in the blood and provide a large buffering capacity owing to their abundance. Deoxygenated Hb is a weaker acid and better buffer than oxygenated.
– with carbon monoxide, forming carboxyhaemoglobin.
– formation of methaemoglobin.
– causing sulphaemoglobinaemia.
– prolonged exposure to raised glucose levels in diabetes mellitus, forming glycosylated Hb.
Normal blood Hb concentration is 13–17 g/dl (men), 12–16 g/dl (women).
Hsia CCW (1998). N Engl J Med; 338: 239–47 – old but still the best
See also, Anaemia; Carbon dioxide transport; Carbon monoxide poisoning; Methaemoglobinaemia; Myoglobin; Oxygen transport; Polycythaemia
Haemoglobinopathies. Diseases of abnormal haemoglobin production (cf. thalassaemias: impaired production of normal haemoglobin). Over 300 variants have been described, mostly due to single amino acid substitutions. Originally named after letters of the alphabet, then after the place of origin of the first patient described. Most are clinically insignificant, but some may lead to acute or chronic haemolysis, and some are associated with impaired O2 binding and secondary polycythaemia. Sickle cell anaemia is the most important; it may be combined with other abnormalities, e.g. haemoglobin C. The latter on its own may cause mild haemolytic anaemia and splenomegaly.
Haemolysis. Abnormal destruction of erythrocytes. Normal red cell survival is about 120 days; bone marrow compensation may restore red cell volume if the lifespan is shortened. Anaemia may result if haemolysis is excessive, bone marrow abnormal, or haematinics (e.g. iron) are deficient. Haemolysis may result in jaundice, decreased haptoglobin concentration (see below) and reticulocytosis.
genetic red cell abnormalities:
– membrane abnormalities, e.g. hereditary spherocytosis, elliptocytosis.
– haemoglobinopathies, thalassaemia.
– enzyme deficiencies, e.g. glucose 6-phosphate dehydrogenase deficiency, pyruvate kinase deficiency.
– immune:
– primary.
– malignancy.
– infection, e.g. viral, mycoplasma.
– drugs, e.g. penicillins, methyldopa, rifampicin, sulphonamides.
– incompatible blood transfusion (including rhesus blood group incompatibility).
– infection, e.g. malaria, generalised sepsis.
– drugs, e.g. sulphonamides, phenacetin.
– trauma, e.g. prosthetic heart valves, extracorporeal circuits. Also associated with red cell damage following contact with vasculitic endothelium (e.g. haemolytic–uraemic syndrome).
– burns.
– paroxysmal nocturnal haemoglobinuria.
extravascular: most common type; involves sequestration of red cells from the circulation.
Haemolytic–uraemic syndrome. Acquired condition involving thrombocytopenia, a microangiopathic haemolytic anaemia and endothelial injury to the renal vasculature, leading to acute kidney injury. Usually occurs in children, especially following diarrhoea (usually due to Shiga toxin-producing Escherichia coli) or upper respiratory infection, but may occur in adults. May occur in cancer, infections and during chemotherapy administration. Closely related to thrombotic thrombocytopenic purpura, but neurological features such as CVA that characterise the latter are uncommon. A similar condition may occur postpartum or in women taking the contraceptive pill.
Treatment is mainly supportive. Although heparin and prostacyclin have been used, their benefit is unproven. Plasmapheresis and immunosuppressive drugs have also been used.
Haemoperfusion. Removal of toxic substances from plasma by adsorption on to special filters, e.g. amberlite resin, activated charcoal granules coated in acrylic gel or cellulose. Performed in poisoning and overdoses, and hepatic failure. Modern devices are extremely efficient; complete removal of toxin from the body is limited by tissue binding. Thus haemoperfusion is most effective for poisons with small volumes of distribution, e.g. barbiturates, disopyramide, theophylline, meprobamate and methaqualone; these are rarely taken in overdose. Tricyclic antidepressants are not removed. Requires vascular cannulation (e.g. femoral vein), extracorporeal circuit and heparinisation. Blood flow of 100–200 ml/min is employed, continued for several hours according to the clinical condition or plasma toxin levels.
Complications: as for dialysis. Thrombocytopenia was common with earlier adsorption columns.
Haemophilia. X-linked recessive coagulation disorder with an incidence (type A) of 1 : 5000–10 000. One-third of cases are new mutations. Predominantly affects males, although female carriers may exhibit mild disease. Female homozygotes almost always die in utero. Results in deficiency of factor VIII (haemophilia A) or IX (haemophilia B; Christmas disease; one-tenth as common), leading to increased bleeding into muscles, joints and internal organs. The intrinsic coagulation pathway is slowed, with activated partial thromboplastin time prolonged; prothrombin and bleeding times are normal. Specific factor VIII/IX assay reveals reduced activity, and von Willebrand factor assay is normal.
• Intensive care/anaesthetic considerations:
– factor VIII is given as a concentrate (preferred), as cryoprecipitate, or as fresh frozen plasma, with haematological advice and monitoring of blood levels. Half-life is 8–12 h; adequate levels are required for at least a week postoperatively. About 15% of patients have circulating antibodies to factor VIII or IX, making control more difficult; eptacog alfa may be useful in such cases.
Desmopressin 0.4 µg/kg iv may transiently increase levels of factor VIII by 3–6 times in mild cases, and tranexamic acid 1 g orally may also be given.
– care should be taken with any invasive procedure, including venesection or arterial blood sampling.
– NSAIDs and antiplatelet drugs should be avoided.
high risk of HIV infection in haemophiliacs given pooled factor VIII before the availability of recombinant factor VIII in the mid/late 1980s and of recombinant factor IX in 1997.
[Stephen Christmas (1947–1993); name of British patient in whom the disease was first described]
Finjvandraat K, Cnossen MH, Leebeek FWG, Peters M (2012). Br Med J; 344: 36–40
Haemorrhage. Physiological effects of acute haemorrhage:
blood volume is reduced, leading to reduced venous return and cardiac output.
arterial BP falls, with activation of the baroreceptor reflex, reduced parasympathetic activity and increased sympathetic activity. Tachycardia, peripheral arterial vasoconstriction (to skin, viscera and kidneys) and venous constriction restore BP, initially. Classified in ATLS guidelines as follows:
– I: up to 15% of blood volume lost (usually little physiological change).
– II: 15–30% lost (tachycardia, peripheral vasoconstriction, postural hypotension).
– III: 30–40% lost (hypotension, mental confusion, maximum tachycardia).
– IV: > 40% lost (cardiovascular collapse and shock). Bradycardia and hypotension may occur with over 20–30% of loss; thought to be vagally mediated, due to cardiac afferent C-fibre discharge caused by ventricular distortion and underfilling.
increased vasopressin secretion and renin/angiotensin system activity causes vasoconstriction, sodium and water retention and thirst.
catecholamine and corticosteroid secretion increase as part of the stress response.
increased movement of interstitial fluid to the intravascular compartment and third space.
increased 2,3-DPG production, increasing tissue O2 delivery.
increased plasma protein synthesis.
increased erythropoietin secretion and erythropoiesis.
Volume restoration takes 1–3 days after moderate haemorrhage, with reduction of haematocrit and plasma protein concentration.
• Features: as for hypovolaemia.
large-bore intravenous cannulae and iv fluid administration:
– cross-matched blood is best (but some benefit in cardiac output and tissue flow is derived from haemodilution).
– colloid maintains intravascular expansion for longer than crystalloid.
– crystalloid: saline is more effective than dextrose.
– CVP and urine output measurement are useful for monitoring volume replacement.
See also, Blood loss, perioperative; Blood transfusion; Colloid/crystalloid controversy; Damage control resuscitation
Haemostasis, see Coagulation
Hagen–Poiseuille equation. For laminar flow of a fluid of viscosity η through a tube of length L and radius r, with pressure gradient P across the length of the tube:
Originally derived by observing flow of liquid through rigid cylinders of different dimensions, with different driving pressures. Applied to blood flow through blood vessels, and gas flow through breathing systems and airways, although these tubes are neither rigid nor perfect cylinders.
[Jean Poiseuille (1797–1869), French physiologist;
Gotthilf HL Hagen (1797–1884), German engineer]
Haldane effect. Increased capacity of deoxygenated blood for CO2 transport compared with oxygenated blood.
increased binding of reduced haemoglobin to CO2, forming carbamino groups (accounts for 70% of the effect).
Half-life (t1/2). The time taken for a substance undergoing decay to decrease by half. Commonly used to describe an exponential process (in which the half-life is constant), but may also refer to a non-exponential process (in which the half-life varies).
radioactive half-life (time taken for half the number of atoms to disintegrate).
drug half-life (time taken for drug concentration to fall by half, whether resulting from redistribution or clearance).
In pharmacokinetics, context-sensitive half-life refers to the time for plasma concentration of a drug to decrease by 50% after terminating an iv infusion that has maintained steady-state plasma concentration. For example, for propofol it is approximately 20 min after 2 h infusion, 30 min after 6 h infusion and 50 min after 9 h infusion. Corresponding figures for midazolam and alfentanil are in the order of 40 min, 70 min and 80 min; for fentanyl: 40 min, 4 h and 5 h. Ultra-short-acting drugs are less affected by ‘context’ (i.e. duration of infusion); for example, for remifentanil it is approximately 3 min, irrespective of the duration of the infusion.
Hall, Richard, see Halsted, William Stewart
Haloperidol. Butyrophenone used as a sedative and antipsychotic drug. Acts by blocking central dopamine receptors. Also acts on cholinergic, serotonergic, histaminergic and α-adrenergic receptors. Has tranquillising effects without impairing consciousness; used to sedate psychotic patients in ICU. Half-life is approximately 20 h.
• Dosage:
1.5–5.0 mg orally bd/tds; up to 100 mg may be needed in severe schizophrenia.
• Side effects include prolonged Q–T syndromes, extrapyramidal symptoms (parkinsonism, dystonia, restlessness and tardive dyskinesia); can trigger the neuroleptic malignant syndrome. Other side effects are similar to those of chlorpromazine, but with less sedation and fewer antimuscarinic effects.
Halothane. 2-Bromo-2-chloro-1,1,1-trifluoroethane (Fig. 80). Inhalational anaesthetic agent, introduced in 1956. Its use rapidly spread because of its greater potency, ease of use, non-irritability and non-inflammability compared with diethyl ether and cyclopropane. Risks of arrhythmias and liver damage on repeated administration (halothane hepatitis) and introduction of newer agents (e.g. sevoflurane, which has replaced halothane as the agent of choice for inhalational induction) have led to a decline in its use. Discontinued for human use in the UK in 2007.
colourless liquid; vapour has characteristic pleasant smell and is 6.8 times denser than air.
SVP at 20°C 32 kPa (243 mmHg).
MAC 0.76%.
supplied in liquid form with thymol 0.01%; decomposes slightly in light.
• Effects:
– smooth rapid induction, with rapid recovery.
– increases cerebral blood flow but reduces intraocular pressure.
– respiratory depressant, with increased respiratory rate and reduced tidal volume.
– bronchodilatation and inhibition of secretions.
– myocardial O2 demand decreases.
– arrhythmias are common, e.g. bradycardia, nodal rhythm, ventricular ectopics/bigemini.
– sensitises the myocardium to catecholamines, e.g. endogenous or injected adrenaline.
– dose-dependent uterine relaxation.
Up to 20% is metabolised in the liver. Metabolites include bromine, chlorine and trifluoroacetic acid; negligible amounts of fluoride ions are produced. Repeat administration after recent use may result in hepatitis.
Fig. 80 Structure of halothane
‘Halothane shakes’, see Shivering, postoperative
Halsted, William Stewart (1852–1922). US surgeon, pioneer of local anaesthetic nerve blocks with Hall and others. He and Hall described blocks of most of the nerves of the face, head and limbs, experimenting on each other and becoming cocaine addicts in the process. Chief of surgery and professor at Johns Hopkins University, where he started the first formal surgical training programme in the USA. Pioneer of aseptic technique, introducing use of rubber gloves during surgery.
Hamburger shift, see Chloride shift
Hanging drop technique. Method of identifying the epidural space, e.g. during epidural or spinal anaesthesia. A drop of saline is placed at the hub of a needle that is advanced towards the epidural space; when the space has been entered the drop is drawn into the needle by the negative pressure within the space. Not always reliable, since negative pressure is not always present.
Haptoglobin. Alpha-globulin synthesised by the liver, that binds free haemoglobin in the blood. Normal serum level is 30–190 mg/dl; this usually binds 100–140 mg free haemoglobin per 100 ml plasma. Haptoglobin–haemoglobin complex is rapidly removed from the circulation by the reticuloendothelial system; if the liver is unable to produce new haptoglobin quickly enough, the plasma haptoglobin level falls. Although the reduction in haptoglobin is used mainly as a sensitive indicator of intravascular haemolysis, it may also occur if haemolysis is extravascular.
Harmonics. Related sine waveforms; the frequency of each is a multiple of the fundamental frequency of the first harmonic, the slowest component of the series. Complex waveforms may be produced by adding higher harmonics to the first (fundamental) harmonic (Fourier analysis). Monitoring equipment must be able to reproduce harmonics of high enough frequency for the signal recorded; e.g. up to the 10th harmonic for many recorders. More harmonics are required for more complex waveforms with higher frequencies, increasing the required frequency response of the monitor concerned, e.g. ECG 0.5–80 Hz, EEG 1–60 Hz, EMG 2–1200 Hz.
Harnesses. Used to secure breathing attachments or facemasks to the patient. May damage soft tissues around the face, and airway obstruction may still occur.
Formerly widely used during ‘mask’ anaesthesia, their use has declined with increasing use of the LMA, though many modern facemasks are still supplied with plastic hooks for attachment. Their disposable silicone/rubber equivalents are used for non-invasive positive pressure ventilation or CPAP.
Hartmann’s solution (Ringer’s lactate; Compound sodium lactate). IV fluid containing sodium 131 mmol/l, potassium 5 mmol/l, calcium 2 mmol/l, chloride 111 mmol/l and sodium lactate 29 mmol/l. pH is 5–7. Originally formulated from Ringer’s solution for fluid replacement and treatment of metabolic acidosis in children, using an isotonic solution containing more sodium than chloride. Lactate is metabolised to glucose and bicarbonate within a few hours, and the hazards of bicarbonate administration avoided. Now widely used as the crystalloid of choice for ECF replacement, since it is more ‘physiological’ in make-up; however, its advantage over saline solutions for routine use has been questioned.
Often avoided in patients with renal failure because of the risk of hyperkalaemia, in sick patients or those with hepatic failure because of the risk of hyperlactataemia (although the clinical relevance of this is unclear), and in diabetics because of the risk of hyperglycaemia (although the actual increase in blood glucose concentration is likely to be small). Due to its calcium content, may cause clotting of stored blood when transfused through a line that has not first been flushed with saline.
Hayek oscillator, see Intermittent negative pressure ventilation
Hb, see Haemoglobin
Hct, see Haematocrit
HDU, see High dependency unit
Head injury. Common cause of morbidity and mortality in trauma, especially in young males; it should be suspected in all trauma cases, especially those involving the chest and neck. Divided into closed or penetrating (the latter having worse outcomes), whilst brain injury can be divided into:
that occurring after the initial injury (secondary) resulting from potentially preventable or treatable causes (e.g. hypoxaemia, hypotension, hypercapnia). Compression due to cerebral oedema or intracerebral, intraventricular, epidural or subdural haemorrhage can be included here, although the first two are usually associated with direct brain injury.
external signs of head injury, e.g. bruising, lacerations. Cervical spine
