S

Published on 09/04/2015 by admin

Filed under Surgery

Last modified 09/04/2015

Print this page

rate 1 star rate 2 star rate 3 star rate 4 star rate 5 star
Your rating: none, Average: 0 (0 votes)

This article have been viewed 1400 times

S

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

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

Saddle block,  see Spinal anaesthesia

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.

• Features:

ent nausea, vomiting, haematemesis, sweating, tinnitus, deafness, confusion, hallucinations. Loss of consciousness is uncommon unless poisoning is severe.

ent hyperventilation results from direct respiratory centre stimulation, possibly via central uncoupling of oxidative phosphorylation. Respiratory alkalosis results. Compensatory renal excretion of bicarbonate results in urinary water and potassium loss with dehydration and hypokalaemia.

ent metabolic acidosis is caused by the salicylic acid, and its metabolic effects (increased production of ketone bodies, lactic acid and pyruvic acid, hyperglycaemia or hypoglycaemia). Thus the urine, initially alkaline, becomes acid.

ent arrhythmias, hypotension.

ent convulsions, pulmonary oedema, hyperthermia and acute kidney injury may occur.

ent impaired coagulation is rarely significant.

• Treatment:

ent general measures as for poisoning and overdose, e.g. O2 therapy, iv fluid administration. Activated charcoal (1 mg/kg) should be given to all patients who have ingested > 150 mg/kg or those who are acutely symptomatic. Additional doses may be given if serum salicylate levels continue to rise.

ent increased elimination may be indicated if plasma levels exceed 500 mg/l (3.6 mmol/l) in adults or 300 g/l (2.2 mmol/l) in children. Techniques include forced alkaline diuresis, dialysis and haemoperfusion.

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

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.

• Scavenging systems consist of:

ent collecting system: usually a shroud enclosing the adjustable pressure limiting valve. For paediatric breathing systems, several attachments have been described, including various connectors and funnels.

ent tubing: standard plastic tubing is usual; all connections should be 30 mm to avoid improper connection to the breathing system.

ent receiving system: incorporates a reservoir to enable adequate removal of gases, even if the volume cleared per minute is less than peak expiratory flow rate. May use rubber bags or rigid bottles. If the system is closed, a dumping valve and pressure-relief valve are required to prevent excess negative or positive pressure, respectively, being applied to the patient’s airway. Vents are often present in rigid reservoirs. Requirements:

– negative pressure: maximum 0.5 cmH2O at 30 l/min gas flow.

– positive pressure: maximum 5 cmH2O at 30 l/min gas flow, and 10 cmH2O at 90 l/min. Ideally, the relief valve should be as near to the expiratory valve as possible.

ent disposal system: may be:

– passive: no external energy supply; the gases pass through wide-bore tubing to the roof of the building, terminating in a ventile. Maximal resistance should be 0.5 cmH2O at 30 l/min. The least efficient system, since it depends on wind direction. Requires a water trap to remove condensed water vapour.

– assisted passive: employs the air-conditioning system’s extractor ducts.

– active: uses a dedicated fan system or ejector flowmeter. Requires a low-pressure high-volume system (able to remove 75 l/min with a peak flow of 130 l/min); thus hospital suction equipment is unsuitable.

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

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.

• Four different approaches are commonly used:

ent posterior: with the patient lying with the side to be blocked uppermost, and the uppermost hip and knee flexed, a line is drawn between the greater trochanter and posterior superior iliac spine. At the line’s midpoint, a perpendicular is dropped 3 cm, and a 12 cm needle introduced at this point, at right angles to the skin. The nerve lies on the ischial spine and is identified using a nerve stimulator (seeking contraction of the hamstrings and muscles of the back of the lower leg and foot). 15–30 ml local anaesthetic agent is injected. Onset of blockade may take 30 min.

ent anterior: with the patient lying supine, a line is drawn between the pubic tubercle and anterior superior iliac spine, and divided into thirds. A perpendicular line is dropped from the junction of the medial and middle thirds. Another line, parallel with the original line, is drawn from the greater trochanter; its intersection with the perpendicular marks the site of needle insertion. A 12 cm needle is directed slightly laterally to encounter the femur, then withdrawn and directed medial to the femur to a depth of 5 cm from the femur’s anterior edge. 15–30 ml solution is injected. This approach is particularly useful if movement is painful, e.g. fractured femur.

ent lithotomy: with the hip and knee on the side to be blocked flexed to 90°, a needle is inserted perpendicular to the skin at the midpoint of a line between the greater trochanter and the ischial tuberosity. 15–20 ml solution is injected at a depth of 4–8 cm. The posterior cutaneous branch (supplying the posterior thigh) may be missed.

ent lateral: with the patient lying supine, a needle is inserted horizontally at a point 2–3 cm below and 4–5 cm distal to the greater trochanter. When the femur is encountered it is withdrawn and redirected posteriorly ~30° and cranially ~30–45° to reach the nerve at 8–10 cm. 20–30 ml solution is injected.

See also, Regional anaesthesia

Scleroderma,  see Systemic sclerosis

Scoliosis,  see Kyphoscoliosis

Scopolamine,  see Hyoscine

Scribner shunt,  see Shunt procedures

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.

• The following drugs have been used for sedation in ICU or for short procedures:

ent opioid analgesic drugs: commonly used on ICU. Provide analgesia and euphoria, and aid toleration of IPPV. All produce respiratory depression. Hypotension is particularly likely if hypovolaemia is present and following rapid iv injection. GIT motility is reduced. Drugs used include:

– morphine 2.5–5 mg boluses (20–60 µg/kg/h infusion). Accumulation of metabolites may occur after prolonged infusion, especially in renal failure. Increased susceptibility to infection has been shown in experimental animals receiving very large doses.

– fentanyl 1–5 µg/kg/h; accumulation readily occurs after prolonged infusion, since its short duration of action initially is due to redistribution, and clearance is slower than that of morphine.

– alfentanil 30–60 µg/kg/h; accumulation is less likely than with fentanyl.

– remifentanil 0.025–0.1 mg/kg/min (with or without an initial dose of e.g. 0.5 mg/kg/min) is also used, either alone or in combination with propofol/midazolam.

ent benzodiazepines: often used in conjunction with opioids. Widely used for short procedures. May produce cardiorespiratory depression, and may accumulate in impaired hepatic/renal function and after prolonged administration. Tachyphylaxis may also occur. Verbal contact with the patient may be impaired. Flumazenil may be used to reverse over-sedation. Commonly used drugs:

– diazepam 2.5–10 mg boluses. It and its metabolites have long duration of action.

– midazolam 2–5 mg boluses (50–200 µg/kg/h infusion).

ent iv anaesthetic agents, e.g.:

– ketamine 5–10 mg boluses (1–2 mg/kg/h infusion). Used during regional anaesthesia, but rarely used in ICU except in asthma.

– thiopental 1–3 mg/kg/h; mainly used in neurological disease (e.g. status epilepticus). Recovery may be prolonged.

– propofol 0.3–4.0 mg/kg/h; allows rapid recovery. For patient-controlled sedation: boluses of 10–20 mg with no background infusion and a lockout of 2–5 min. Target-controlled infusion (TCI) is also used: 0.5–3.0 µg/ml target with or without patient-controlled increases as required. Propofol is licensed for 3 days’ sedation of adults (but should be avoided in children). It is licensed for longer use in neurosurgical patients. May cause propofol infusion syndrome.

– etomidate: no longer used in ICU because of adrenal suppression.

ent inhalational anaesthetic agents:

– N2O up to 70% is commonly used during regional anaesthesia, but haematological side effects preclude prolonged or frequent use.

– isoflurane has been used on ICU with good results, although high plasma levels of fluoride ions have been reported after prolonged use. May be administered using highly efficient delivery devices without the need for anaesthetic machines.

ent others:

– clonidine and dexmedetomidine have been used successfully for the sedation of patients on ICU.

– clomethiazole, droperidol, chlorpromazine; rarely used. Chloral hydrate, 30–50 mg orally/rectally repeated as required, may be useful in children.

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

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.

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 FIO2. 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:

image

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 sensory fibres enter the spinal cord through the dorsal root, their cell bodies lying in the dorsal root ganglia. Subsequent pathways (Fig. 139):

ent dorsal columns: carry impulses concerned with proprioception (movement and joint position sense), vibration and discriminative touch:

– first-order neurones turn medially and ascend in the ipsilateral posterior columns (the fasciculus gracilis and cuneatus) to the lower medulla, where they synapse with cells in the cuneate or gracile nuclei.

– second-order neurones cross (decussate) to the contralateral side of the medulla and ascend in the medial lemniscus to the ventral posterior nucleus of the thalamus.

– third-order neurones project to the somatosensory cortex.

ent spinothalamic tract: carries impulses concerned with pain, temperature, non-discriminative touch and pressure:

– first-order neurones synapse in the dorsal horn of the spinal cord (most nociceptive Aδ- and C-fibres terminate in laminae I–II whereas Aβ fibres terminate in laminae III–IV).

– second-order neurones carrying pain and temperature cross within one segment of their origin, whereas those carrying touch and pressure may ascend for several segments before crossing. They ascend in the spinothalamic tract; in the medulla, this forms the spinal lemniscus, which ascends to the ventral posterior nucleus of the thalamus.

– third-order neurones project to the somatosensory cortex.

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.

• Signs of sensory pathway loss:

ent peripheral nerve lesion: complete loss of sensation in the nerve’s distribution (although the zone of loss may be limited because of overlap between nerves).

ent posterior root lesion: pain and paraesthesia are experienced in the dermatomal distribution. If the root involves a reflex arc, the reflex will be diminished or lost.

ent posterior column lesion: ipsilateral loss of position and vibration sense with preservation of pain, touch and temperature sensation.

ent spinothalamic tract lesion: contralateral loss of pain and temperature sensation.

ent brainstem and thalamus lesions: upper brainstem or thalamic lesions may cause complete hemisensory disturbance with loss of postural sense, light touch and pain sensation. ‘Pure’ thalamic lesions may result in central pain.

ent sensory cortex lesions: paraesthesia may be felt, with or without impaired sensation, e.g. inability to distinguish between heat and pain, or inability to identify objects by touch.

[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

Buy Membership for Surgery Category to continue reading. Learn more here