S-100β protein.  Calcium-binding protein present in glial cells, studied as an early marker of damage to the blood–brain barrier, e.g. after CVA, head injury, cardiac surgery and neurosurgery. A normal level reliably excludes significant CNS injury. Metabolised in the kidney with a half-life of ~25 min, the serum concentration is usually negligible but increases after brain injury, although it is thought that S-100β may also be produced from other tissues and its relationship with functional impairment is uncertain.

Cata JP, Abdelmalak B, Farag E (2012). Br J Anaesth; 107: 844–58

S wave,  Downward deflection following the R wave of the ECG (see Fig. 59b; Electrocardiography). Its size usually decreases from V₂ to V₆; the deepest wave is normally less than 30 mm. Prominence in standard leads I, II and III (S₁S₂S₃ pattern) may be normal in young people but may be associated with right ventricular hypertrophy. May also be seen in MI along with other changes.

See also, QRS complex

SA node,  Sinoatrial node, see Heart, conducting system

Sacral canal.  Cavity, 10–15 cm long and triangular in section, running the length of the sacrum, itself formed from five fused sacral vertebrae (Fig. 136). Continuous cranially with the lumbar vertebral canal. The anterior wall is formed by the fused bodies of the sacral vertebrae, and the posterior walls by the fused sacral laminae. Due to failure of fusion of the fifth laminar arch, the posterior wall is deficient between the cornua, forming the sacral hiatus, which is covered by the sacrococcygeal membrane (punctured during caudal analgesia). Congenital variants of fusion are common, e.g. deficient fusion of several laminae; this is thought to be a contributing cause of unreliability of caudal analgesia. The canal contains the termination of the dural sac at S2, the sacral nerves and coccygeal nerve, the internal vertebral venous plexus and fat. Its average volume in adults is 32 ml in females and 34 ml in males.

Crighton IM, Barry BP, Hobbs GJ (1997). Br J Anaesth; 78: 391–5

Sacral nerve block,  see Caudal analgesia

Sacral plexus.  Supplies the pelvic and hip muscles, and the skin of the buttock and posterior thigh. Lies on piriformis muscle on the posterior wall of the pelvis, deep to the pelvic fascia, and is formed from the anterior primary rami of L4–S4 (Fig. 137). Its major branches are the sciatic, pudendal and gluteal nerves.

See also, Sciatic nerve block

Saddle block,  see Spinal anaesthesia

Safe transport and retrieval (STaR).  Course conceived by the Advanced Life Support Group and first run in 1998. Teaches a systematic approach to the safe transfer and retrieval of critically ill and injured patients. Aimed at doctors, nurses and paramedics.

See also, Transportation of critically ill patients

Salbutamol.  β-Adrenergic receptor agonist, used mainly as a bronchodilator drug. Relatively selective for β₂-receptors, although it does cause β₁-receptor stimulation. Undergoes extensive first-pass metabolism if given orally, thus usually administered by inhalation or iv. Produces bronchodilatation within 15 min; effects last 3–4 h. May also reduce the release of histamine and inflammatory mediators from mast cells sensitised with IgE, hence its particular use in asthma.

Also used as a tocolytic drug in premature labour and to improve cardiac output in low perfusion states, via β₂-receptor-mediated smooth muscle relaxation in the uterus and blood vessels respectively.

Salicylate poisoning.  Usually acute but may be chronic, especially in children.

Mortality of acute overdose is approximately 2%; mortality of chronic overdose about 25%.

Pearlman BL, Gambhir R (2009). Postgrad Med; 121: 162–8

See also, Forced diuresis

Salicylates.  Group of NSAIDs derived from salicylic acid. Aspirin (acetylsalicylic acid) is the most commonly used; others are available but are less potent, e.g. sodium salicylate. Have anti-inflammatory and antipyretic effects; they inhibit both central and peripheral synthesis of prostaglandins. Inhibit platelet and vascular endothelial cyclo-oxygenase; at low dosage, they selectively inhibit platelet cyclo-oxygenase. They are thus used as antiplatelet drugs. Effects on platelets are irreversible, lasting until new platelets are synthesised (7–10 days).

Used for mild-to-moderate pain, pyrexia, rheumatic fever, rheumatoid arthritis, and peripheral and coronary artery disease. Contraindicated in gout as they may impair excretion of uric acid.

Absorbed rapidly from the upper GIT after therapeutic dosage, with peak plasma levels within 2 h of ingestion. Absorption is determined by the composition of tablets, intestinal pH and gastric emptying. About 90% protein-bound, they compete with other substances for protein binding sites, e.g. thyroxine, penicillin, phenytoin. Metabolised in the liver and excreted mainly in the urine, especially if the latter is alkaline. Half-life is about 15 min, but is very dependent on the dose taken.

Contraindicated in children < 16 years and patients with peptic ulcer disease; used with caution in those with coagulation disorders or taking anticoagulant drugs.

Saline solutions.  IV fluids containing sodium chloride, used extensively to replace sodium and ECF losses, e.g. in dehydration, and perioperatively. A 0.9% solution is most commonly used (‘physiological saline’, often erroneously called ‘normal saline’); other saline-containing solutions include Hartmann’s solution, Ringer’s solution and dextrose/saline mixtures. Twice ‘normal’ saline (1.8%) is used in hyponatraemia, and up to 7.5% solutions have been used (largely experimentally) in hypovolaemic shock.

Administration of large volumes of saline may result in hyperchloraemic acidosis, the clinical significance of which is unclear.

See also, Hypertonic intravenous solutions; Normal solution

Samples, statistical.  Parts of populations, selected for statistical tests or analysis. In order to represent the true population, samples should be as large as possible to ensure appropriate power, and free of bias; i.e. should be random. Matched samples refer to groups matched for possible confounding variables, allowing better comparison of the desired measurements. Optimum matching occurs when subjects act as their own controls (i.e. measurements are paired).

See also, Clinical trials; Randomisation; Statistics

Sanders oxygen injector,  see Injector techniques

Saphenous nerve block,  see Ankle, nerve blocks; Knee, nerve blocks

SAPS,  see Simplified acute physiology score

Sarcoidosis.  Systemic disease, possibly caused by an infective agent or immunological derangement, characterised by non-necrotising granuloma formation. The lungs or hilar lymph nodes are affected in over 80% of patients, but the disease may involve the eyes, skin, musculoskeletal system, abdominal organs, heart or nervous system. Often acute in onset and self-limiting.

Diagnosed on clinical grounds, supported by tissue biopsy, CXR, hypercalcaemia (due to derangement of vitamin D metabolism), raised angiotensin converting enzyme levels and positive Kveim test (granuloma formation following intradermal injection of sarcoid tissue suspension).

Anaesthetic and ICU considerations include the possibility of pulmonary fibrosis, cardiac failure, heart block, laryngeal fibrosis, renal failure and hypercalcaemia. Corticosteroids are often prescribed.

[Morten A Kveim (1892–1967), Norwegian pathologist]

Dempsey OJ, Paterson EW, Kerr KM, Denison AR (2009). Br Med J; 339: 620–5

SARS,  see Severe acute respiratory syndrome

Saturated vapour pressure (SVP).  Pressure exerted by the vapour phase of a substance, when in equilibrium with the liquid phase. Indicates the degree of volatility; e.g. for inhalational anaesthetic agents, diethyl ether (SVP 59 kPa [425 mmHg]) is more volatile and easier to vaporise than halothane (SVP 32 kPa [243 mmHg]). SVP increases with temperature, therefore SVPs of volatile agents are quoted at standard temperature (usually 20°C). At boiling point, SVP equals atmospheric pressure.

See also, Vapour pressure

Scalp, nerve blocks.  Local anaesthetic infiltration is usually performed with added adrenaline, because of the rich vascular supply of the scalp. Injection is performed first in the subcutaneous tissue above the aponeurosis (where nerves and vessels lie), then below. Infiltration in a band around the head, above the ears and eyebrows, provides anaesthesia of the scalp. Individual branches of the maxillary nerve may also be blocked. The occipital nerves supplying the posterior scalp may be blocked by infiltrating between the mastoid process and occipital protuberance on each side.

Scavenging.  Removal of waste gases from the expiratory port of anaesthetic breathing systems; desirable because of the possible adverse effects of exposure to inhalational anaesthetic agents. Adsorption of volatile agents using activated charcoal (Aldasorber device) has been used but does not remove N₂O.

Workplace exposure limits set out in COSHH regulations for Great Britain and Northern Ireland are 100 ppm N₂O, 50 ppm enflurane/isoflurane and 10 ppm halothane (each over an 8-h period). Maximum permitted levels vary between countries; e.g. in the USA, the National Institute for Occupational Safety and Health has recommended an 8-h time-weighted average limit of 2 ppm for halogenated anaesthetic agents in general (0.5 ppm together with exposure to N₂O).

See also, Environmental safety of anaesthetists; Pollution

SCCM,  see Society of Critical Care Medicine

Schimmelbusch mask,  see Open-drop techniques

Sciatic nerve block,  Used for surgery to the lower leg, often combined with femoral nerve block, obturator nerve block and lateral cutaneous nerve of the thigh block (see Fig. 66; Femoral nerve block). May also be performed to provide analgesia after fractures, or sympathetic nerve block of the foot.

The sciatic nerve (L4–S3) arises from the sacral plexus, leaving the pelvis through the greater sciatic foramen beneath the piriformis muscle, and between the ischial tuberosity and the greater trochanter of the femur. It becomes superficial at the lower border of gluteus maximus, and runs down the posterior aspect of the thigh to the popliteal fossa, where it divides into tibial and common peroneal nerves. It supplies the hip and knee joints, posterior muscles of the leg and skin of the leg and foot below the knee, except for the medial calf. The posterior cutaneous nerve of the thigh runs close to it and is usually blocked by it.

See also, Regional anaesthesia

Scleroderma,  see Systemic sclerosis

Scoliosis,  see Kyphoscoliosis

Scopolamine,  see Hyoscine

Scribner shunt,  see Shunt procedures

SCUF,  Slow continuous ultrafiltration, see Ultrafiltration

SDD,  see Selective decontamination of the digestive tract

Second.  SI unit of time; defined according to the frequency of radiation emitted by caesium-133 in its lowest energy (ground) state.

Second gas effect.  Increased alveolar concentration of one inhalational anaesthetic agent caused by uptake of a second inhalational agent. Most marked when the second gas occupies a large volume, e.g. N₂O. Analogous but opposite to the Fink effect at the end of anaesthesia.

Second messenger.  Intracellular substance (e.g. cAMP, calcium ions) linking extracellular chemical messengers (first messengers) with the physiological response. G protein-coupled receptors are often involved in second messenger systems.

Sedation.  State of reduced consciousness in which verbal contact with the patient may be maintained. Used to reduce discomfort during unpleasant procedures, e.g. regional anaesthesia, dental surgery, endoscopy, cardiac catheterisation, and on ICU. For short procedures, drugs of short duration of action causing minimal cardiorespiratory depression are preferable. Best control is usually achieved with iv administration, although other routes may be used, e.g. oral premedication. Routine monitoring should be employed during procedures as for general anaesthesia. Drugs may be given by intermittent bolus, or by continuous infusion; the latter is easier to titrate. The level of sedation required depends on the individual patient and the procedure performed. Patient-controlled sedation has been used during procedures performed under local or regional anaesthesia; the patient uses a patient-controlled analgesia device containing e.g. propofol as required.

On ICU, sedative and analgesic drugs are given to reduce pain, distress and anxiety, and to aid tolerance of tracheal tubes, IPPV, tracheal suction and physiotherapy. Cardiovascular depression is undesirable, although respiratory depression may be an advantage if IPPV is required. Long-term administration is often required; thus side effects not seen after brief administration may occur, and drugs with long half-lives may accumulate. The desired end-point is usually a calm, cooperative patient who can respond to commands, with deeper levels of sedation provided for stimulating procedures. Sedation scoring systems have been devised to assist titration of drugs.

Neuromuscular blocking drugs are sometimes used in ICU to facilitate IPPV, especially if chest compliance is reduced or ICP is raised. Their use has declined in recent years because of the risk of paralysis with concurrent inadequate sedation, increased risk from accidental disconnection, possible increased incidence of DVT, PE, critical illness polyneuropathy and impaired communication. Atracurium and vecuronium are most commonly used.

NSAIDs and regional techniques may also be used to provide analgesia in ICU.

Patel SB, Kress JP (2012). Am J Respir Crit Care Med; 185: 486–97

Sedation scoring systems.  Used in intensive care to assess the level of sedation of patients in order to balance its beneficial (reduced stress, cardiovascular stability, ventilator synchrony) and adverse (increased risk of ventilator-associated pneumonia, deep vein thrombosis) effects. Provide an opportunity to titrate the level of sedation against predefined end-points (e.g. assessments of consciousness, agitation and/or ventilator synchrony). Other parameters assessed include pain, anxiety, muscle tone and reaction to tracheal suction. Most systems use single numerical scores:

[Michael AE Ramsay, US anaesthetist]

De Jonghe B, Cook D, Appere-De-Vecchi C, et al (2000). Intensive Care Med; 26: 275–85

Seebeck effect,  see Temperature measurement

Seldinger technique.  Method for percutaneous cannulation of a blood vessel, described in 1953. A needle is inserted into the vessel, and a guide-wire passed through it. After removal of the needle, the cannula is introduced into the vessel over the wire, which is then removed. Refinements include the use of a dilator passed over the wire to enlarge the hole made by the needle, before the cannula is inserted. Widely used for central venous cannulation; favoured by many as being safer and more reliable than using cannula-over-needle techniques, although more costly.

Also used to cannulate other body cavities, e.g. the trachea in percutaneous tracheostomy formation, the chest for insertion of a chest drain or the abdominal cavity in paracentesis.

[Sven-Ivar Seldinger (1921–1998), Swedish radiologist]

Selective decontamination of the digestive tract (SDD; Selective parenteral and enteral antisepsis regimen, SPEAR).  Technique for preventing infections in patients requiring ventilatory support on ICU. SDD aims to prevent colonisation of the GIT by potentially pathogenic organisms, based on the premise that most infections on ICU are endogenous.

Non-absorbable antibacterial drugs (e.g. tobramycin, colistin, amphotericin, neomycin) are administered to the pharynx/mouth/upper GIT, whilst another (e.g. cefotaxime) is administered iv. Sparing of the normal anaerobic GIT organisms prevents overgrowth by pathogens. SDD significantly reduces nosocomial pneumonia, with some evidence of mortality benefit; however, concerns over inducing antibiotic resistance have not been fully addressed. Its place in ICU continues to be debated.

Schulz MJ, Haas LE (2011). Crit Care; 15: R18

Selective serotonin reuptake inhibitors (SSRIs).  Antidepressant drugs, introduced in 1987 and increasingly replacing tricyclic antidepressant drugs as the main group of drugs used in depression and other disorders. Inhibit the presynaptic reuptake of 5-HT in the CNS, leading to an increase in 5-HT activity. Include citalopram, escitalopram, fluoxetine, fluvoxamine, paroxetine and sertraline; they have similar actions and are metabolised in the liver with half-lives of about a day (4–6 days for fluoxetine).

Have fewer side effects than tricyclic antidepressants since muscarinic, dopamine, histamine and noradrenergic receptors are unaffected. However, GIT upset, insomnia and agitation may occur; the syndrome of inappropriate antidiuretic hormone and impaired platelet function have been reported. In overdose, severe adverse effects are uncommon, although the serotonin syndrome may occur if tricyclics or monoamine oxidase inhibitors are also taken.

May cause hepatic enzyme inhibition (by competing with other drugs for the same metabolic pathways), thus increasing the action of certain tricyclics, type Ic antiarrhythmic drugs (especially lipid-soluble β-adrenergic receptor antagonists), phenytoin and benzodiazepines. Increased bleeding may occur in warfarin therapy. Concurrent administration of drugs which have 5-HT reuptake blocking effects (e.g. pethidine) may provoke the serotonin syndrome.

Selenium.  Trace element found in meat, chicken and fish; normal intake ~60–75 µg/day. Selenoproteins are antioxidants and are involved in certain biological reactions, e.g. conversion of thyroxine to triiodothyronine. Low blood selenium levels have been recorded in ICU patients, especially those with septic shock. Low selenium levels are associated with a high ICU mortality; the replenishment of plasma selenium is associated with a decrease in nosocomial infections and a decreased mortality in patients with sepsis.

Berger MM, Shenkin A (2007). Crit Care Med; 35: 306–7

Self-inflating bags.  Rubber or silicone bags used for IPPV, which reinflate when released after compression. Thus may be used for IPPV without requiring an external gas supply, e.g. during draw-over anaesthesia, transfer of ventilated patients or CPR. May be thick-walled or lined with foam rubber. Usually assembled with a non-rebreathing valve at the outlet and a one-way valve at the inlet; thus fresh air is drawn in during refilling. O₂ may be added through a port at the inlet; a reservoir bag may also be added to the inlet to increase F_IO₂. Available in adult and paediatric sizes. Bellows may be used in a similar way, but are less convenient to use.

Sellick’s manoeuvre,  see Cricoid pressure

Semon’s law,  see Laryngeal nerves

Sengstaken–Blakemore tube.  Double-cuffed gastric tube designed to compress gastro-oesophageal varices, thereby controlling bleeding. Passed via the mouth into the stomach; the distal balloon is then inflated with 150–250 ml air, preventing accidental removal. The proximal balloon is then inflated to 30–40 mmHg (4–5 kPa), compressing the varices. Traction has been advocated but is rarely used. Newer versions include channels for aspiration of gastric and oesophageal contents (Fig. 138); the latter may be aspirated continuously to reduce pulmonary soiling. Thus four lumina may be present:

Usually kept inflated for 12–24 h; the oesophageal balloon is deflated first. Careful placement is essential to avoid airway obstruction, pulmonary aspiration, ischaemic necrosis of gastric mucosa or oesophageal rupture. The tubes are very uncomfortable.

[Robert W Sengstaken and Arthur H Blakemore (1879–1970), US surgeons]

Sensitivity.  In statistics, the ability of a test to exclude false negatives. Equals:

See also, Errors; Predictive value; Specificity

Sensory evoked potentials,  see Evoked potentials

Sensory pathways.  The sensory system includes the special senses, visceral sensation and general somatic sensation. The latter is divided into:

Free nerve endings may be associated with nociception. Some nerve endings are ‘specialised’, e.g. Meissner’s corpuscles (touch), Pacinian corpuscles (vibration and joint position) and Ruffini corpuscles (joint position). The last two may be involved with muscle spindles.

The primary somatosensory area of the cerebral cortex is in the postcentral gyrus, although there is a large distribution of sensory fibres in other areas. Regions of greatest importance (e.g. face, mouth, hands) have a disproportionately greater representation than other areas.

[Georg Meissner (1829–1905), German anatomist; Filippo Pacini (1812–1883), Italian anatomist; Angelo Ruffini (1864–1929), Italian histologist]

See also, Dermatomes; Spinal cord injury

Sepsis.  SIRS as a result of proven or suspected infection (i.e. invasion of normally sterile host tissue by micro-organisms and the inflammatory response to their presence). ‘Severe sepsis’ is defined as sepsis plus organ dysfunction, hypoperfusion or hypotension, and replaces the now obsolete term septicaemia (bacteraemia is the presence of viable circulating bacteria). A major cause of organ failure in ICU, severe sepsis is directly or indirectly responsible for 75% of all ICU deaths.

Most ICU infections are endogenous, caused by colonisation of the patient’s GIT by pathogenic organisms. Gram-negative bacteria (e.g. Escherichia coli, klebsiella, pseudomonas and proteus species) have traditionally been most commonly responsible, because of their widespread presence, their tendency to acquire resistance to antibacterial drugs and their resistance to drying and disinfecting agents. Gram-positive bacteria (e.g. streptococci, staphylococci) are increasingly common, especially associated with invasive cannulation; other organisms (e.g. fungi) may also be responsible. The inflammatory response involves cytokines, nitric oxide, thromboxanes, leukotrienes, platelet activating factor, prostaglandins and complement. Endothelial and neutrophil adhesion molecule expression increases, resulting in cellular infiltration into the tissues.

Complications include septic shock and multiple organ failure, including acute lung injury, acute kidney injury, hepatic failure, pancreatitis and diabetes mellitus, DIC, cardiac failure and coma. GIT haemorrhage is common; prophylaxis includes proton pump inhibitors and H₂ receptor antagonists.

Eissa D, Carton EG, Buggy DJ (2010). Br J Anaesth; 105: 734–43

See also, Catheter-related sepsis; Fungal infection in the ICU; Nosocomial infection; Sepsis-related organ failure assessment; Sepsis score; Sepsis severity score

Sepsis-related organ failure assessment (SOFA).  Scoring system devised in 1994 to describe quantitatively and objectively the degree of organ dysfunction in sepsis over time. Intended to improve the understanding of organ dysfunction/failure and to assess the effect of particular therapies on its progression. The function of six different organ systems (respiratory, cardiovascular, central nervous, coagulation, hepatic and renal systems) is weighted (each scored 1–4) according to the degree of physiological derangement observed. Minimum SOFA score is 6; maximum 24.

Vincent JL, Moreno R, Takala J, et al (1996). Intensive Care Med; 22: 707–10

Sepsis score.  Index of severity of sepsis, devised in 1983; assigns scores according to local infection, pyrexia, systemic response and laboratory results. Now rarely used.

Elebute EA, Stoner HB (1983). Br J Surg; 70: 29–31

Sepsis severity score.  Index of severity of sepsis, devised in 1983 by assigning scores of 1–5 according to the degree of impairment of each of the following organ systems: lung, kidney, coagulation, CVS, liver, GIT and neurological. The three highest (worst) scores are then squared to produce the final score.

Stevens LE (1983). Arch Surg; 118: 1190–2

Sepsis syndrome.  Obsolete term for the systemic response to infection.

See also, Sepsis; Septic shock; Septicaemia; Systemic inflammatory response syndrome

Septic shock.  Hypotension (or the requirement for inotropic or vasopressor drugs) despite adequate fluid resuscitation, with evidence of perfusion abnormalities (e.g. lactic acidosis, oliguria), associated with sepsis. Initial features include hyperthermia, tachycardia, tachypnoea, hypotension and vasodilatation with a hyperdynamic circulation and increased cardiac output. In later stages, or if hypovolaemia or poor myocardial function is present, hypotension with vasoconstriction supervenes. Mortality is about 50%, although it varies with patients’ characteristics and the nature of the sepsis. Most cases are caused by bacteria (approximately equally split between Gram-positive and -negative, although traditionally associated with Gram-negative organisms); other organisms may also be responsible.

Risk factors include: age (< 10 years and > 70 years); diabetes mellitus; alcoholic liver disease; ischaemic heart disease; malignancy; immunosuppression; prolonged hospital stay; invasive monitoring; tracheal intubation; and prior use of antibacterial agents. The underlying pathophysiology is as for sepsis; microvascular abnormalities supervene, including impaired autoregulation, altered blood cell morphology, increased endothelial permeability and opening of arteriovenous shunts.

Eissa D, Carton EG, Buggy DJ (2010). Br J Anaesth; 105: 734–43

Septicaemia,  see Sepsis

Sequential analysis,  see Statistical tests

Serotonin,  see 5-Hydroxytryptamine

Serotonin reuptake inhibitors,  see Selective serotonin reuptake inhibitors

Serotonin syndrome.  Impaired mental state, increased muscle activity and autonomic instability arising from excessive 5-HT activity in the brainstem and spinal cord. Seen in selective serotonin reuptake inhibitor (SSRI) overdose, especially in combination with other antidepressant drugs (especially monoamine oxidase inhibitors). Has also been reported after intraoperative use of methylene blue (a potent inhibitor of monoamine oxidase) in a patient taking SSRIs. Also associated with the use of tramadol, pethidine and cocaine. Features include confusion, agitation, convulsions, myoclonus, rigidity, hyperreflexia, fever, diarrhoea, hyper- or hypotension and tachycardia. DIC, renal and cardiac failure may also occur. Treatment is supportive; 5-HT antagonists, e.g. methysergide, cyproheptadine, have been used. Usually lasts for < 24 h but deaths have been reported.

A washout period of several weeks has been suggested between monoamine oxidase inhibitor and SSRI therapy.

Boyer EW, Shannon M (2005). N Engl J Med; 352: 1112–20

Severe acute respiratory syndrome (SARS).  Infectious respiratory condition caused by a new coronavirus, first reported in East Asia in early 2003 and thought to have spread via air travellers to Europe and North America. Has mostly affected previously healthy adults, with an incubation period of 2–11 days. Spread mainly via airborne droplets, with most cases of transmission thought to involve close exposure to an infectious individual. Features include high fever initially with malaise, myalgia and headache; after 3–7 days dry cough and dyspnoea may occur, leading to acute respiratory failure in 10–20% of cases and a mortality ranging from 1% in patients < 24 years to > 50% in those > 65 years. CXR, initially normal, may show focal interstitial infiltrates which may become generalised. Thrombocytopenia and leucopenia are common; raised liver function tests may occur but renal function usually remains normal. Treatment is largely supportive, although the following have been used empirically:

Staff require protection from infection since several cases of transmission to healthcare workers have occurred.

Lai TS, Yu WC (2010). Clin Med; 10: 50–3

Severinghaus electrode,  see Carbon dioxide measurement

Sevoflurane.  1,1,1,3,3,3-hexafluoroisopropyl fluoromethyl ether (Fig. 140). Inhalational anaesthetic agent, first synthesised in 1968 but not introduced in the UK until 1995 because of the development of isoflurane in preference.

Under 5% metabolised in the liver to hexafluoroisopropanol and inorganic fluoride ions, the rest being excreted by the lungs. High levels of fluoride have never been reported, even after prolonged surgery, but avoidance in renal impairment has been suggested. Inducers of the particular cytochrome P₄₅₀ enzyme involved (e.g. isoniazid, alcohol) increase metabolism of sevoflurane, but barbiturates do not.

0.5–3.0% is usually adequate for maintenance of anaesthesia, with higher concentrations for induction. Tracheal intubation may be performed easily with spontaneous respiration. Considered the agent of choice for inhalational induction in paediatrics because of its rapid and smooth induction characteristics. Has also been used for the difficult airway, including airway obstruction.

See also, Vaporisers

Shivering, postoperative.  Tremors were first described after barbiturate administration, but they may occur following all types of general anaesthesia. Traditionally said to be more common following halothane (‘halothane shakes’). Rarer in elderly patients due to decreased thermoregulatory control. May increase metabolic rate by up to six times and triple O₂ consumption. Can also aggravate postoperative pain, damage surgical wounds and increase intraocular and intracranial pressures. Damage to teeth may occur, especially in the presence of an oral airway.

EMG studies suggest that postoperative shivering differs from shivering due to cold. It has been suggested that anaesthetic agents suppress descending pathways which normally inhibit spinal reflexes; this may be more likely than a response to intraoperative hypothermia, although the latter may be of importance if severe.

Shivering after epidural anaesthesia is common, and is thought to be caused by differential nerve blockade, either suppressing descending inhibition of spinal reflexes or allowing selective transmission of cold sensation. Shivering is rare in spinal anaesthesia, where blockade is more dense. Warming of epidural injectate has produced conflicting results. Epidural administration of opioid analgesic drugs, e.g. sufentanil 50 µg, fentanyl 25 µg, pethidine 25 mg, may be an effective remedy.

De Witte J, Sessler DI (2002). Anesthesiology; 96: 467–84

Shock.  Syndrome, originally described by Crile, in which tissue perfusion is inadequate for the tissues’ metabolic requirements. Sympathetic compensatory mechanisms may preserve organ perfusion initially, but subsequent organ dysfunction may lead to irreversible organ damage and death.

Division into hypovolaemia, myocardial failure and peripheral vascular failure has been suggested as being more indicative of underlying mechanisms. Thus shock may arise from inadequate cardiac output or maldistribution of blood flow; the latter has been increasingly implicated by studies of O₂ delivery () and total body O₂ consumption (). A decrease in is thought to represent maldistribution rather than an absolute decrease in blood flow. In cardiogenic shock both and cardiac output are reduced; in septic shock they may both increase initially. Features depend on the aetiology but include hypotension, tachycardia, oliguria and metabolic acidosis. MODS may follow, with acute kidney injury and ARDS. Hepatic, gastrointestinal and pancreatic impairment, and DIC may occur.

Mortality exceeds 50% for cardiogenic and septic shock.

Shock index (SI).  Ratio of heart rate to systolic blood pressure; has been used to identify and monitor haemorrhage in trauma patients. An elevated shock index (> 0.9) has been suggested as an indication for admission to ICU.

Shock lung,  see Acute respiratory distress syndrome

Shunt.  One extreme form of mismatch, causing hypoxaemia. Refers to the actual amount of venous blood bypassing ventilated alveoli and mixing with pulmonary end-capillary blood (cf. venous admixture, the calculated amount of shunt required to produce the observed arterial PO₂).

Physiological shunt (venous admixture) = shunt-like effect of mismatch + anatomical shunt (actual shunt). The latter includes pathological shunt and normal mixing of bronchial and Thebesian venous blood with oxygenated pulmonary venous blood.

Hypoxaemia due to shunt responds poorly to increased F_IO₂, since the O₂ content of pulmonary end-capillary blood is already near maximum, because of the shape of the oxyhaemoglobin dissociation curve. Some benefit is derived from increased dissolved O₂. Thus the amount of shunt may be estimated from the response to breathing high concentrations of O₂, assuming a haemoglobin concentration of 10–14 g/100 ml, arterial PCO₂ of 3.3–5.3 kPa (25–40 mmHg) and arteriovenous O₂ difference of 5 ml/100 ml (Fig. 141). Amount of shunt may also be estimated from the shunt equation.

[Adam Thebesius (1686–1732), German physician]

Shunt equation.  

Allows calculation of shunt. Derived as follows. Total pulmonary blood flow equals , made up of blood flow to unventilated alveoli () and blood flow to ventilated alveoli (; Fig. 142).

In unit time, the volume of O₂ leaving the lungs equals the volume of O₂ in blood draining ventilated alveoli plus the volume of O₂ in shunted blood. Or,

Thus or or

Therefore

Arterial and venous O₂ contents may be estimated thus:

where P_aO₂ and S_aO₂ = arterial PO₂ and haemoglobin saturation respectively,

and = mixed venous PO₂ and haemoglobin saturation respectively,

S = volume of O₂ dissolved in 100 ml blood per kPa applied O₂ tension (0.0225) or mmHg (0.003),

Hb = haemoglobin content in g/100 ml,

1.34 = Hüfner’s constant.

End-capillary O₂ content cannot be measured directly, but is estimated from calculation of the alveolar air equation:

where P_AO₂ = ‘ideal’ alveolar PO₂, and saturation is assumed to be 100%.

Shunt procedures.  Performed to provide access to the circulation for haemodialysis and related procedures, thus requiring the capacity for high flow rates of blood both out of and back into the circulation. May involve:

[Belding H Scribner (1921–2003), Seattle nephrologist]

Shy–Drager syndrome,  see Autonomic neuropathy

SI units,  Units of the Système International d’Unités, see Units, SI

SIADH,  see Syndrome of inappropriate antidiuretic hormone secretion

Siamese twins,  see Conjoined twins

Sick Doctor Scheme.  Scheme set up in 1981 in the UK by the Association of Anaesthetists and Royal College of Psychiatrists, to encourage voluntary reporting of sick doctors practising anaesthesia. The anonymous reporter, having contacted the Association, is given the name and telephone number of a referee. The latter contacts an appointed psychiatrist from another region, who in turn contacts the sick doctor. A similar scheme (National Counselling Service for Sick Doctors) is now available to doctors from all specialties. Intended as an alternative to the more formal scheme available via the Department of Health (previously involving appropriate action taken via a subcommittee [‘three wise men’ procedure]; more recently replaced by a framework involving the National Clinical Assessment Service) and General Medical Council (assesses doctors on health and performance as well as conduct).

A scheme of the same name exists in Ireland, to help doctors affected by substance abuse.

Sick euthyroid syndrome (Non-thyroidal illness syndrome).  Abnormal thyroid function tests occurring in critically ill patients. The most common pattern is low triiodothyronine (T₃) with normal or raised thyroxine (T₄) and thyroid stimulating hormone (TSH). Low T₃ and T₄ are generally associated with more severe critical illness and worse prognosis. Most patients are clinically euthyroid. Thought to result from impaired pulsatile secretion of TSH, reduced peripheral conversion of T₄ to T₃ and reduced plasma protein binding.

It is not clear if the changes seen are an appropriate response to severe illness or a maladaptive response that should be treated; correction of deficits with thyroid hormone replacement has not shown consistent survival benefit.

Bello G, Ceaichisciuc I, Silva S, Antonelli M (2010). Minerva Anestesiol; 76: 919–28

Sick sinus syndrome.  Syndrome caused by impaired sinoatrial node activity or conduction; may lead to periods of severe bradycardia with intermittent loss of P waves or sinus arrest, and may alternate with periods of SVT or AF (bradycardia–tachycardia syndrome; bradytachy syndrome). Although it usually occurs in elderly patients with ischaemic heart disease, it is also a major cause of sudden death in children and young adults. May be precipitated by anaesthesia and result in refractory bradycardia or even asystole. Requires cardiac pacing if diagnosed preoperatively or if it occurs perioperatively.

Staikou C, Chondrogiannis K, Mani A (2012). Br J Anaesth; 108: 730–44

See also, Heart, conducting system

Sickle cell anaemia.  Haemoglobinopathy, first described in 1910 in Chicago. Caused by substitution of glutamic acid by valine in the sixth amino acid from the N-terminal of haemoglobin β chains. Inherited as an autosomal gene; heterozygotes (genotype HbAS; sickle cell trait) possess both normal (HbA) and abnormal (HbS) haemoglobins (though they may also possess other abnormal haemoglobin combinations [e.g. HbSC]) or β thalassaemia (Sβ); homozygotes (HbSS) possess only abnormal haemoglobin. Thought to have originated from spontaneous genetic mutation, with subsequent selection owing to the relative resistance against falciparum malaria conferred by sickle cell trait. Most common in West Central Africa, North-East Saudi Arabia and East Central India, but has been described in Southern Mediterranean populations. Incidence of HbSS in US Blacks is < 1%; incidence of HbAS is 8–10%.

Deoxygenated HbS polymerises and precipitates within red blood cells, with distortion and increased rigidity. Sickle-shaped red cells are characteristic. The distorted cells increase blood viscosity, impair blood flow and cause capillary and venous thrombosis and organ infarction. They have shortened survival time. O₂ affinity of dissolved HbS is normal, but overall affinity is reduced if some of the HbS is polymerised. HbS polymerises at PO₂ of 5–6 kPa (40–50 mmHg); thus HbSS patients are continuously sickling. HbAS patients’ red cells contain both HbS and HbA and sickle at 2.5–4.0 kPa (20–30 mmHg).

Diagnosis is by detection of HbS in the blood. The Sickledex test involves addition of reagent to blood, with observation for turbidity. It detects HbS but provides no information about other haemoglobins. A sodium metabisulphite test induces sickling in susceptible cells, which are then counted. Haemoglobin electrophoresis is the definitive method of determining the nature of the haemoglobinopathy.

Sickle cells are usually present in peripheral blood in HbSS.

de Montalembert M (2008). Br Med J; 337: 626–30

SID,  see Strong ion difference

Siggaard-Andersen nomogram.  Diagram derived from analysis of many blood samples, showing the plot of log arterial PCO₂ against plasma pH, with base excess, standard bicarbonate and buffer base illustrated as additional lines (Fig. 143). Allows determination of arterial PCO₂ by equilibrating a blood sample with two known concentrations of CO₂, and measuring the sample pH at each concentration. The points are plotted on the diagram and joined by a line, and the PCO₂ read from the vertical scale according to the pH of the original sample. Alternatively, if arterial PCO₂ can be measured directly, a single measurement of pH and PCO₂, together with haemoglobin concentration (since haemoglobin is a major blood buffer), allows determination of the derived data. Modern blood-gas machines automatically perform the required calculations, making such plotting unnecessary.

[Ole Siggaard-Andersen, Danish biochemist]

Sigh,  see Intermittent positive pressure ventilation

Significance,  see Statistical significance

Sildenafil (Viagra).  Orally active phosphodiesterase inhibitor, selective for cyclic guanine monophosphate (cGMP)-specific phosphodiesterases. Licensed for use in pulmonary hypertension and male erectile dysfunction. Catastrophic interactions with nitrates (e.g. GTN) have been reported, resulting in severe hypotension and death; thus a history must be obtained in suspected ischaemic heart disease before administering nitrates. Tadalafil and vardenafil are related drugs.

Simplified acute physiology score (SAPS).  Scoring system used to assess severity of illness by determining the degree of deviation of physiological variables from normal values. Originally incorporating 14 variables and excluding pre-existing disease, a modified version (SAPS II) has been developed in which 12 variables are weighted according to age and underlying disease. SAPS III uses a new, improved model for risk adjustment. Used in a similar way to APACHE.

Capuzzo M, Moreno RP, Le Gall JR (2010). Curr Opin Crit Care; 16: 477–81

See also, Mortality/survival prediction on intensive care unit

Simpson, James Young (1811–1870).  Scottish obstetrician; Professor of Midwifery at Edinburgh. The first to administer an anaesthetic for obstetrics in 1847, using diethyl ether. Following a suggestion by Waldie later that year, he used chloroform for the same purpose. Encountered stiff opposition from the clergy and others, who maintained that painful childbirth was either God’s will, beneficial to the patient, or both; this continued until Snow’s administration of chloroform to Queen Victoria in 1853 (‘chloroform à la reine’). Helped popularise chloroform as the replacement for ether. Was made baronet in 1866.

[David Waldie (1813–1889), Scottish-born Liverpool doctor and chemist]

McKenzie AG (2011). Anaesthesia; 66: 438–40

Simulators.  Training devices that allow the duplication of specific clinical scenarios. Useful in the development of diagnostic and therapeutic skills, decision-making, team training, analysing tasks and errors and assessing risks. Allow prospective and repeated observation and analysis of actions rather than retrospective assessment. Individual components, e.g. mannikins, may be used to teach specific skills (part-task trainers), or combined within the setting of an entire operating suite with monitoring equipment and controlled with computers (high-fidelity simulation), often interacting through a mathematical model.

Are now widely used in areas other than anaesthesia, e.g. obstetrics, emergency medicine and surgery.

Despite best efforts, simulators may not always reflect real conditions accurately. For instance, some activities may be easier to perform on simulators than in the operating room; conversely, some may be more difficult. Reality is further impeded by the need to model average ‘patients’ who may not respond in the ‘extreme’ ways of some real patients; equally, subjects’ responses may be different when they are aware that they are working with a simulator. The cost of sophisticated simulators and the labour-intensive staffing requirements are further disincentives. Nevertheless, simulation has become an established part of training programmes in many countries, and has also been studied as a means of assessing practitioners.

Castanelli DJ (2009) Anaesth Intensive Care; 37: 903–10

See also, Crisis resource management

SIMV,  Synchronised intermittent mandatory ventilation, see Intermittent mandatory ventilation

Simvastatin,  see Statins

Single-pass albumin dialysis,  see Liver dialysis

Sinoatrial node,  see Heart, conducting system

Sinus arrhythmia.  Normal phenomenon (especially in young people) characterised by alternating periods of slow and rapid heart rates. The ECG shows sinus rhythm with irregular spacing of normal complexes. Most commonly related to respiration, with a rapid rate at end-inspiration and a slower rate at end-expiration. A number of mechanisms have been proposed, including: activation of pulmonary stretch receptors during inspiration, causing inhibition of the cardioinhibitory centre via vagal afferents; changes in intrathoracic pressure causing stretching of the sinoatrial node, producing cardiac accelerations during inspiration; and lower intrathoracic pressure during inspiration, causing reduced cardiac output, leading to an increase in heart rate mediated by the baroreceptor reflex. May also involve direct impulse conduction between medullary respiratory and cardiac neurones. Also seen in patients treated with digoxin. Abolished by atropine.

Sinus bradycardia.  Usually defined as sinus rhythm at less than 60 beats/min. The ECG shows normal P waves and QRS complexes occurring at a slow rate.

If it occurs, the stimulus should be stopped. It may be treated with anticholinergic drugs (e.g. atropine), β-adrenergic receptor agonists or cardiac pacing, but treatment is only required if accompanied by symptoms, hypotension or escape beats.

Sinus rhythm.  Normal heart rhythm in which each P wave is followed by a QRS complex on the ECG; i.e. each impulse originates in the sinoatrial node, which has the fastest inherent rhythmicity of all cardiac pacemaker cells. Normal heart rate is usually defined as 60–100 beats/min.

See also, Cardiac cycle; Heart, conducting system; Sinus arrhythmia; Sinus bradycardia; Sinus tachycardia

Sinus tachycardia.  Usually defined as sinus rhythm at over 100 beats/min. The ECG shows regular normal P waves and QRS complexes at a rapid rate.

Reduces the time available for ventricular filling and coronary blood flow; it may precipitate myocardial ischaemia if severe. Treatment is usually directed at the cause; β-adrenergic receptor antagonists may be required if the patient is at risk of myocardial ischaemia.

Sinusitis.  Infection of the nasal sinuses of the skull. May occur as a consequence of upper respiratory tract infection, trauma or, especially relevant to ICU, prolonged tracheal intubation; has been reported in 2–40% of patients requiring IPPV. Up to 10 times more common if nasotracheal or nasogastric tubes are in place; thought to be related to obstruction of drainage through the sinus ostia (although in a third of cases the contralateral side is affected). Also more common in immunosuppressed and diabetic patients. Usually affects the maxillary or sphenoid sinuses, although ethmoid and frontal sinusitis may also occur (and may result in cerebral venous thrombosis).

May present with non-specific features of sepsis; diagnosed by CT scanning (although plain X-rays may be helpful), ± antral puncture and aspiration. Ultrasound examination may be useful, but requires specialised equipment. Organisms involved are usually Gram-negative bacteria, staphylococci or anaerobes. Management includes extubation, antibacterial drugs ± surgical drainage. Antihistamines and decongestants have also been used. Usually resolves within a week of extubation.

See also, Intubation, complications of

SIRS,  see Systemic inflammatory response syndrome

Skin diseases.  Anaesthetic considerations may be related to:

In addition, anaesthetic agents may precipitate cutaneous lesions (e.g. in adverse drug reactions, bullous eruption following barbiturate poisoning, porphyria).

Skull.  The upper part contains the brain, whilst the lower anterior portion forms the facial skeleton:

In addition, branches of the first cranial nerve pass through the cribriform plate’s perforations.

See also, Mandibular nerve blocks; Maxillary nerve blocks; Ophthalmic nerve blocks; Orbital cavity

Skull X-ray.  Useful investigation for the detection of linear and depressed skull fractures following head injury, for classifying facial trauma and planning of maxillofacial surgery. Although the presence of a fracture increases the likelihood of intracranial damage, significant injury may be present with a normal X-ray. Investigation of choice for demonstrating basal skull fractures, which are poorly visualised by CT scanning. Pneumocephalus is easily evident on a plain skull X-ray.

Sleep.  Naturally occurring state of unconsciousness; the response to external stimuli is decreased, but the subject may usually be readily roused. Two patterns are described:

In a typical night’s sleep, a young adult rapidly passes through stages 1 and 2, spending about 60–90 min in stages 3 and 4. A period of REM sleep follows, lasting 60–90 min. This cycle repeats, thus providing about five episodes of REM sleep per night (25% of total sleep time). Sleep disruption is common in the ICU and may be related to:

Sleep deprivation may result in ICU delirium, increased catabolism (due to increased corticosteroid secretion and insulin resistance), fatigue and difficulty in weaning from ventilators.

Hardin KA (2009). Chest; 136: 284–94

Sleep apnoea/hypopnoea.  Cessation (apnoea) or reduction of > 30% (hypopnoea) of breathing for > 10 s during sleep. Resultant hypoxaemia and hypercapnia causes arousal, thus disrupting normal sleep architecture. Affects 5–10% of the adult population. May have a central mechanism (caused by lack of respiratory drive, e.g. Ondine’s curse) or may be obstructive (obstructive sleep apnoea; OSA). OSA is caused by decreased tone of the pharyngeal muscles during deep sleep, resulting in intermittent upper airway obstruction.

Screening questionnaires are used to identify those at high risk; formal diagnosis requires sleep studies, with polysomnography (monitoring of respiratory airflow, chest and abdominal movements, EEG and oximetry). OSA severity is classified according to the apnoea–hypopnoea index (number of apnoeas/hypopnoeas divided by the number of hours of sleep): 5–15 = mild; 15–30 = moderate; > 30 = severe.

Treatment includes weight loss, nasal CPAP and removal of tonsils if enlarged. Uvulopharyngopalatoplasty (UVPP) is of dubious benefit. Tracheostomy may be indicated in severe cases.

Adesanya AO, Lee W, Greilich NB, Joshi GP (2010). Chest; 138: 1489–98

Slow-reacting substance-A,  see Leukotrienes

Smallpox,  see Biological weapons

Smoke inhalation.  Resultant pulmonary insufficiency is the commonest cause of death in patients admitted to hospital with burns.

Further respiratory impairment may occur if infection and acute lung injury supervene.

See also, Nitrogen, higher oxides of

Smoking.  Common cause of cardiovascular and respiratory pathology in surgical and non-surgical patients.

Smokers are more likely to have increased sputum production and retention, bronchospasm, coughing, atelectasis and chest infection perioperatively. Poor wound and bone healing is also more common.

Stopping smoking is thought to be beneficial preoperatively, in order to minimise its acute adverse effects. Effects of carbon monoxide and nicotine are significantly reduced after 12–24 h abstinence; up to 6–8 weeks is thought to be necessary for restoration of ciliary and immunological activity.

Sweeney BP, Grayling M (2009). Anaesthesia; 64: 179–86

See also, Carbon monoxide poisoning

Snake bites,  see Bites and stings

Snow, John (1813–1858).  Pioneer of English anaesthesia, born in York. Moved to London in 1836. Developed the science and art of anaesthesia, describing five stages of anaesthesia in 1847. Designed inhalers for diethyl ether and chloroform, and wrote two famous textbooks on the use of these agents (his book on chloroform was published posthumously). Widely regarded as the expert in his field, he administered chloroform to Queen Victoria during childbirth in 1853 and 1857. Also famous for demonstrating that cholera was spread by contaminated drinking water, not by foul air, as previously believed. Removal of the Broad Street water pump handle on his suggestion is said to have stopped the London epidemic of 1854. One of the heraldic supporters of the Royal College of Anaesthetists (with Clover).

Society of Critical Care Medicine (SCCM).  Founded in 1970 to support the specialty of critical care as a separate but interdisciplinary entity, with Critical Care Medicine as its official journal. Supports research, education and provision of resources.

Soda lime.  Mixture used for CO₂ absorption in anaesthetic breathing systems, composed of calcium hydroxide (~90%), sodium hydroxide (4–5%), potassium hydroxide (traditionally 1%; in the UK modern preparations do not contain potassium hydroxide), silicates (for binding; less than 1%) and indicators. Used with 14–19% water content. CO₂ in solution reacts with sodium (± potassium) hydroxides to form the respective carbonates, which then react with calcium hydroxide to produce calcium carbonate, replenishing sodium and potassium hydroxides. Heat and water are also produced during the reaction. Exhaustion of its activity is indicated by dyes; several have been used, but the most common one changes from pink to white.

Provided in granules of size 4–8 mesh (will pass through a mesh of 4–8 strands per inch in each axis; i.e. pore size of 1/16–1/64 in²). Canisters should be tightly packed to reduce channelling of gases through large gaps. The total volume of space between granules should equal the volume of the granules themselves. Dust may be inhaled using older systems, especially the ‘to-and-fro’ system. Large canisters containing up to 2 kg soda lime are commonly employed.

Known to react with trichloroethylene, with the risk of neurological damage. The modern inhalational anaesthetic agents, especially sevoflurane, may react with soda lime if the latter is warm and very dry. Compound A, carbon monoxide, formic acid and formaldehyde may be produced. Compound A is a particular product of sevoflurane, leading to fears over its use in circle systems, although evidence of toxic levels of compound A within such systems has not been found. Significant levels of carbon monoxide have been reported. Furthermore, the temperature in the absorber may increase to dangerous levels and there may be some absorption of the volatile agent itself. The minimal level of moisture that will prevent such reactions is 2% for sodium hydroxide and 4.7% for potassium hydroxide, leading to the latter’s removal from modern preparations in the UK. Normal use of circle systems is not thought to result in such low levels of moisture, but they have been found after prolonged passage of dry gas through the absorber, e.g. at the start of a Monday morning operating session if gases are left running over the weekend.

Attempts to prevent the soda lime drying out include shutting off anaesthetic machines after use, changing the soda lime regularly and not relying on colour changes to indicate dehydration, checking for unusually hot absorption canisters or unexpectedly low concentrations of volatile agent, and addition of zeolites that can physically trap water, or inorganic chlorides that crystallise water within the soda lime. A new mixture (calcium hydroxide lime) consisting of calcium hydroxide with calcium chloride (plus calcium sulphate and polyvinylpyrrolidone to improve hardness and porosity) has been developed which does not contain sodium or potassium hydroxide and does not react with any of the currently used volatile agents.

See also, Baralyme

Sodium (Na⁺).  Principal cation in the ECF, accounting for 90% of the osmotically active solute in plasma and interstitial fluid. Thus the prime determinant of ECF volume. Total body content is about 4000 mmol, of which 50% is in bone, 40% in ECF, and 10% intracellular. About 70% is available for exchange. Normal plasma levels: 135–145 mmol/l. Of central importance in the function of excitable cells, e.g. concerning membrane potentials and action potentials.

Actively absorbed from the small intestine and colon, facilitated by aldosterone and the presence of glucose in the gut lumen. The kidney filters approximately 26 000 mmol Na⁺/day, of which 99.5% is reabsorbed by passage through the nephron (mostly at the proximal convoluted tubule). Reabsorption is influenced by renal tubular hydrostatic and oncotic gradients, aldosterone, adrenocortical hormones, atrial natriuretic hormone and the rate of secretion of hydrogen and potassium ions.

See also, Hypernatraemia; Hyponatraemia

Sodium bicarbonate,  see Bicarbonate

Sodium calcium edetate.  Chelating agent, used in the treatment of acute and chronic lead poisoning. Has also been used successfully in poisoning with copper and radioactive materials.

Sodium citrate.  Non-particulate antacid, widely used preoperatively to increase gastric pH in patients at risk of aspiration of gastric contents, e.g. before general anaesthesia in obstetrics. Thought to be less harmful than magnesium trisilicate if inhaled. Effective for 30–50 min following oral intake of 30 ml 0.3 molar solution.

Also used to relieve discomfort from urinary tract infection by raising urinary pH.

Sodium clodronate,  see Bisphosphonates

Sodium cromoglicate (Cromoglycate).  Drug used in the prophylaxis of asthma; of no value in acute attacks. Thought to stabilise mast cells by preventing calcium ion entry, thus preventing IgE-triggered release of inflammatory mediators. Particularly useful in allergic and exercise-induced asthma in children. Should be taken regularly as a powder, aerosol or nebulised solution, usually 10–20 mg 4–8 times daily. Generally less effective than corticosteroids.

See also, Bronchodilator drugs

Sodium dichloroacetate.  Activator of pyruvate dehydrogenase, resulting in increased oxidation of lactate to acetylcoenzyme A and CO₂. Has been used to treat lactic acidosis, although randomised trials have not found an increase in survival.

Sodium nitrite,  see Cyanide poisoning

Sodium nitroprusside (SNP).  Vasodilator drug, used as an antihypertensive drug, e.g. in hypotensive anaesthesia. Also used in cardiac failure. Presented as a powder for reconstitution in 5% dextrose. Unstable in solution, with decomposition to highly coloured products. Solutions require protection from light and should be used within 24 h of preparation.

Reacts with thiol groups in vascular smooth muscle and converted to nitrite, which reacts with hydrogen ions to produce nitric oxide. Acts mainly on arteries, although veins are also affected. Thus reduces SVR, maintaining cardiac output and tissue perfusion. Also reduces myocardial O₂ consumption whilst increasing coronary blood flow, although coronary steal has been reported. Compensatory tachycardia is common. Hepatic blood flow remains constant, whilst renal blood flow and cerebral blood flow increase. Active within 30 s of administration. Broken down non-enzymatically within red blood cells (catalysed by haemoglobin) to produce five cyanide ions from each molecule, some of which combine with haemoglobin to form methaemoglobin; the remainder are converted to thiocyanate in the liver by rhodonase and then excreted in the urine. Plasma half-life of SNP is about 2 min.

Sodium/potassium pump.  Protein pump present in every cell membrane, responsible for active transport of sodium out of cells and potassium into cells. The protein is an enzyme which catalyses hydrolysis of ATP to ADP, providing the energy required for the transport. Consists of two α subunits (mw 95 000) that extend through the membrane and provide the binding site for ATP, and two β subunits (mw 40 000). Three sodium ions are transported for every two potassium ions, creating a net negative charge within the cell. Required for maintenance of cellular membrane potential and electrolyte composition. Inhibited by cardiac glycosides.

Sodium thiosulphate,  see Cyanide poisoning

Sodium valproate.  Anticonvulsant drug used for all forms of epilepsy. Acts mainly by blocking neuronal sodium channels but also by inhibiting calcium channels in thalamic neurones and enhancing GABA activity. Rapidly absorbed by mouth and largely protein-bound (90%), its half-life is approximately 12 h.

SOFA,  see Sepsis-related organ failure assessment

Solubility.  Extent to which a substance dissolves in another substance.

See also, Partition coefficient

Solubility coefficients.  Expression of solubility. Two coefficients are commonly used:

For solubility of inhalational anaesthetic agents, the Ostwald solubility coefficient (at 37°C) is usually used as it is independent of pressure.

[Robert WE Bunsen (1811–1899) and Wilhelm Ostwald (1853–1932), German chemists]

Solvent abuse.  Form of substance abuse involving the intake (usually by inhalation) of a variety of solvents used in glues, paints and similar products; include toluene, petroleum products and carbon tetrachloride. Acute problems may include depressed consciousness and arrhythmias, the latter probably related to myocardial sensitisation to endogenous catecholamines. Sudden death has occurred. Specific organ damage (renal, hepatic) may occur with specific substances, e.g. toluene after prolonged usage. Management is largely supportive.

Somatostatin (Growth hormone inhibiting hormone).  Hormone secreted by the pancreas, GIT mucosa and hypothalamus. Exists in two forms, with either 14 or 28 amino acid residues. Also a neurotransmitter in the brain and spinal cord (especially substantia gelatinosa, where it may be involved in pain transmission – somatostatin has been shown to produce analgesia when injected epidurally). Other actions include:

Analogues (lanreotide and octreotide) have been used: to control diarrhoea and flushing in the carcinoid syndrome, possibly via inhibition of 5-HT release; in the management of bleeding oesophageal varices; and in the management of acromegaly.

Sonoclot,  see Coagulation studies

Sore throat, postoperative.  Reported in up to 90% of cases in some studies, and in up to 25% of patients following spontaneous breathing via a facemask.

Also common after tracheal intubation in the ICU, especially after prolonged IPPV.

McHardy FE, Chung F (1999). Anaesthesia; 54: 444–53

Sotalol hydrochloride.  Water-soluble non-selective β-adrenergic receptor antagonist and class III antiarrhythmic drug, available for oral and iv administration. Used for prophylaxis and treatment of SVT and VT.