Nabilone.  Cannabinoid antiemetic drug, acting on CB₁ and CB₂ cannabis receptors, used in chemotherapy-induced nausea and vomiting. Has also been used in palliative care.

Nalbuphine hydrochloride.  Opioid analgesic drug and opioid receptor antagonist, synthesised in 1968. Partial agonist at kappa and sigma opioid receptors, and partial antagonist at mu receptors. Used for premedication, anaesthesia and treatment of pain. Active within 2–3 min of iv, or 15 min of im injection. Half-life is about 5 h. Undergoes hepatic metabolism and excreted renally. Side effects such as vomiting are thought to be less than with morphine, although maximal analgesia attainable is also less. Psychomimetic effects are less problematic than with pentazocine. Withdrawn from the UK market in 2003.

Nalmefene hydrochloride.  Opioid receptor antagonist, introduced in the USA in 1995. Longer half-life (10.8 h) than naloxone, thus less likely for opioid effects to recur following reversal.

Nalorphine hydrochloride/hydrobromide.  Opioid analgesic drug and opioid receptor antagonist, synthesised in 1941. Partial agonist at kappa and sigma opioid receptors, and antagonist at mu receptors. Psychomimetic effects are common at analgesic doses (5–10 mg). No longer available.

Naloxone hydrochloride.  Opioid receptor antagonist, synthesised in 1961. N-Allyl derivative of oxymorphone. Although it has a high affinity for the mu receptor, it has no intrinsic activity. Used to reverse unwanted effects of opioid analgesic drugs, e.g. sedation, respiratory depression, spasm of the biliary sphincter. Also reverses opioid-mediated analgesia. Reverses the effects of pentazocine but not buprenorphine. Used to reverse ventilatory depression and pruritus following spinal opioids, without reversing analgesia. Also used in poisoning and overdoses due to other depressant drugs, e.g. alcohols, benzodiazepines, barbiturates, although its efficacy is disputed. Reportedly useful in septic shock, increasing BP and cardiac output; the mechanism is unclear but may involve increase of endogenous catecholamine release or antagonism of increased levels of endorphins that occur in sepsis. Effective within 1–2 min of iv injection, with a half-life of 1–2 h; thus depressant effects of opioid analgesic drugs may recur after a few hours. Metabolised in the liver and excreted mainly renally.

NALS.  Neonatal Advanced Life Support, see Neonatal Resuscitation Program

Naltrexone hydrochloride.  Opioid receptor antagonist, synthesised in 1965. Derived from naloxone, with similar actions but longer duration (24 h after a single dose). Used in the treatment of opioid and alcohol dependence.

Naproxen.  NSAID derived from propionic acid. Has a favourable side-effect profile among NSAIDs (although not as potent as ibuprofen), and can be given just twice daily.

Narcotic drugs.  Strictly, drugs which induce sleep, but the term usually refers to morphine-like drugs. Preferred terms include opiates, opioids and opioid analgesic drugs.

Nasal inhalers.  Used instead of facemasks for dental anaesthesia. Designed to fit over the nose, leaving the mouth free. During induction of anaesthesia, the patient is instructed to breathe through the nose. During anaesthesia, a mouth pack prevents mouth breathing. Now rarely used.

[Victor Goldman (1903–1993), London anaesthetist]

Nasal positive pressure ventilation,  see Non-invasive positive pressure ventilation

Nasogastric intubation.  Performed for enteral nutrition, or gastric drainage. Fine-bore tubes are used for the former, usually inserted using a wire stylet, which is removed after placement. Larger tubes (e.g. 10–16 Ch) are used for gastric drainage, e.g. following abdominal surgery or in intestinal obstruction. They may be placed in the awake patient (who aids placement by swallowing or sipping water) or unconscious patient (e.g. after induction of anaesthesia, either before or after tracheal intubation). Placement can often be performed blindly, and may be aided by passage through a plain nasal tracheal tube placed into the pharynx or by prior transient inflation of the upper oesophagus via a tightly fitting facemask. Placement may require direct vision using a laryngoscope and forceps (the oesophagus lies posterior to the larynx and to the left of the midline). Correct placement is confirmed by aspiration of gastric contents (should be tested for acidity), auscultation over the left hypochondrium during injection of air, abdominal X-ray or palpation by the surgeon during surgery. If already in place, withdrawal of the tube before induction of anaesthesia has been suggested, to avoid increasing gastro-oesophageal reflux or rendering cricoid pressure inefficient. However, this is rarely done.

National Confidential Enquiry into Patient Outcome and Death (NCEPOD).  Ongoing study originally commissioned by the Association of Anaesthetists of Great Britain and Ireland, together with the Association of Surgeons of Great Britain and Ireland, and published in 1987 as the Confidential Enquiry into Perioperative Deaths (CEPOD). The first UK study to involve both anaesthetists and surgeons, it analysed all 4000 NHS deaths occurring within 30 days of surgery (excluding obstetric and cardiac surgery) in three regions during 1986. The first national Report (NCEPOD; 1989) focused on children under 10 years; subsequent Reports have focused on particular aspects, e.g. deaths following specific surgical or interventional procedures or in specific age groups, out-of-hours operating, acute kidney injury.

The scheme now includes independent hospitals and also involves the Royal Colleges of Anaesthetists, Obstetricians and Gynaecologists, Ophthalmologists, Pathologists, Physicians, Radiologists and Surgeons, and the Faculties of Dental Surgery and Public Health Medicine of the Royal Colleges of Surgeons and Physicians respectively. The name changed in 2002 to the National Confidential Enquiry into Patient Outcome and Death, reflecting extension of NCEPOD’s remit to include physicians and primary care and to review near misses as well as deaths. Although an independent body, NCEPOD is funded mainly by the Department of Health.

National Halothane Study,  see Hepatitis

National Institute of Academic Anaesthesia (NIAA).  Established in 2008 by the Royal College of Anaesthetists, Association of Anaesthetists of Great Britain and Ireland, British Journal of Anaesthesia and Anaesthesia, to further the academic profile of the specialty of anaesthesia and promote high-quality research. Coordinates the assessment and awarding of anaesthetic research grants within the UK, and houses the Health Services Research Centre (HSRC) which coordinates national, outcome-based projects.

Mahajan RP, Reilly CS (2012). Br J Anaesth; 108: 1–3

National Institute for Health and Clinical Excellence (NICE).  NHS Special Health Authority for England and Wales, established in 1999 (as the National Institute for Clinical Excellence) to provide authoritative, evidence-based and reliable guidance on current ‘best practice’. Its guidance is derived from independent assessments of clinical evidence combined with cost-effectiveness analyses, and covers both individual health technologies (including medicines, medical devices, diagnostic techniques and procedures) and the clinical management of specific conditions. In 2005, NICE took on the functions of the Health Development Agency to become the National Institute for Health and Clinical Excellence (though still known as NICE). Is thus responsible for providing national guidance on the promotion of good health and the prevention and treatment of ill health.

National Patient Safety Agency (NPSA).  NHS Special Health Authority, formed in 2001 to coordinate reports of adverse events or ‘near misses’ and their analysis. Operated three main services until its abolishment in 2012:

See also, Confidential Enquiry into Maternal Deaths; National Confidential Enquiry into Patient Outcome and Death

Natriuretic hormone,  see Atrial natriuretic peptide

Nausea,  see Postoperative nausea and vomiting; Vomiting

NCEPOD,  see National Confidential Enquiry into Patient Outcome and Death

Near-drowning.  Defined as initial survival following immersion in liquid, usually water; death at the time of immersion may be due to anoxia (drowning) or cardiac arrest caused by sudden extreme lowering of temperature (immersion syndrome). Secondary drowning refers to death following near-drowning after a period of relative wellbeing and is usually due to ARDS/acute lung injury.

Autopsy following drowning reveals little or no lung water in 15% of cases (dry drowning); laryngospasm following initial laryngeal contamination has been suggested. In 85% of cases, pulmonary aspiration of water occurs (wet drowning); this may involve:

Both types cause pulmonary oedema and hypoxaemia. Haemodynamic changes due to fluid shifts are rare; thus in practice the type of water may have little clinical significance.

Other adverse factors include hypothermia, aspiration of gastric contents and predisposing conditions, e.g. alcoholism or drug abuse, trauma, epilepsy, MI, CVA.

Complications include ARDS, cerebral oedema, acute kidney injury, pneumonia, pancreatitis, acidosis and shock. Sepsis is especially likely if the water is contaminated.

Recovery has been reported after up to 60 min immersion followed by prolonged CPR, especially in children and if hypothermic. Hypoxic brain injury may occur.

Szpilman D, Bierens JJLM, Handley AJ, Orlowski JP (2012). N Engl J Med; 366: 2102–10.

Near infrared oximetry/spectroscopy (NIRS).  Monitoring technique based on the principle that light in the near infrared spectrum (650–900 nm wavelength) transmits through biological tissues. Increasingly used to image biological events in the cerebral cortex. Photons produced by a laser photodiode are directed into the skull; whilst many are reflected and dispersed, a proportion is transmitted. Coloured compounds within the tissues (chromophores), especially oxyhaemoglobin, deoxyhaemoglobin and oxidised cytochrome oxidase, have characteristic absorption spectra. The emergent light intensity is detected and a computer converts the changes in light intensity into changes in chromophore concentration. Clinical applications include monitoring of cerebral oxygenation and cerebral blood flow and volume, e.g. in neurosurgery, cardiac surgery and head injury.

Murkin JM, Arango M (2009). Br J Anaesth; 103 (suppl 1); i3–13

See also, Functional imaging

Nebulisers.  Devices used to provide a suspension of droplets in a gas, for administration of inhaled drugs or humidification. Droplets of 5 µm are deposited in the trachea and bronchi; those of 1 µm pass to alveoli and may impair gas exchange. Thus the ideal droplet size is between 1 and 5 µm.

Neck, cross-sectional anatomy.  At the level of C6, major anatomical structures within the layer of skin, fat and subcutaneous tissue may be described in terms of fascial layers (Fig. 113):

See also, Carotid arteries; Tracheobronchial tree

Necrotising enterocolitis (NEC).  Necrosis of GIT mucosa (especially terminal ileum, caecum and ascending colon) seen in neonates, usually within the first week of life. Prevalence is up to 8% in premature and low-birth-weight babies; predisposing factors include asphyxia, hypotension and umbilical catheterisation. Mucosal damage follows hypoperfusion and ischaemia, leading to abdominal distension, vomiting and faecal blood and mucus, although the onset may be insidious. Pallor, bradycardia, jaundice, intestinal perforation and DIC may occur. Plain abdominal X-ray shows dilated loops of bowel and intramural gas bubbles.

Management is largely supportive, with iv fluids, IPPV, correction of anaemia, antibacterial drugs (including anaerobic cover), probiotic agents and TPN. Surgery may be required if perforation occurs or there is no improvement despite medical therapy. Quoted mortality ranges from 10% to 50%. Survivors commonly exhibit impaired psychomotor development.

Wu SF, Caplan M, Lin HC (2012). Pediatr Neonatol; 53:158–63

Necrotising fasciitis.  Uncommon deep-seated infection of subcutaneous tissue, resulting in destruction of fat and fascia. Predisposing factors include immunosuppression, alcoholism, diabetes, peripheral vascular disease, surgery, penetrating injuries (which may be minor) and varicella infection, although it may affect young healthy individuals. Systemic upset is thought to result from bacterial toxins, endogenous cytokines and other inflammatory mediators. May be rapidly fatal unless aggressively treated. May be caused by:

[Jean A Fournier (1832–1914), Paris dermatologist]

Ustin JS, Malangoni MA (2011). Crit Care Med; 39: 2156–62

Needles.  Christopher Wren described injection via a quill and bladder in 1659. Metal tubes and stylets were subsequently used, but the hypodermic cannula and trocar were first described by Rynd in 1845. Different sizes and types are available for different uses, e.g. for iv/hypodermic use, epidural and spinal anaesthesia. Short-bevelled needles are traditionally preferred for regional anaesthesia. Hollow needles are not required for acupuncture or electrical stimulation/recording.

Needle size is described by a wire gauge classification (G; Stubs gauge; Birmingham gauge), which originally referred to the number of times the wire was drawn through the draw plate (Table 30). It differs slightly from the American and Standard wire gauges. Internal diameter varies according to different materials and needle strengths. The system is also used for iv cannulae. For hypodermic needles, colour-coding is mandatory in the UK for certain sizes: 26 G brown; 25 G orange; 23 G blue; 22 G black; 21 G green; 20 G yellow; 19 G cream.

[Sir Christopher Wren (1633–1723), English scientist and architect; Francis Rynd (1801–1861), Irish surgeon; Peter Stubs (1756–1806), English toolmaker and innkeeper]

Needlestick injury,  see Environmental safety of anaesthetists

NEEP,  see Negative end-expiratory pressure

Nefopam hydrochloride.  Centrally acting analgesic drug, unrelated to opioid analgesic drugs and NSAIDs. Inhibits reuptake of 5-HT, noradrenaline and dopamine. Has similar analgesic potency to NSAIDs. Peak action occurs 1–2 h after im injection. Drowsiness and respiratory depression may occur, but less than with opioids.

Evans MS, Lysakowski C, Tramèr MR (2008). Br J Anaesth; 101: 610–17

Negative end-expiratory pressure (NEEP).  Adjunct to IPPV, popular in the 1960s–70s as a method of reducing the adverse cardiovascular effects of IPPV by maintaining a subatmospheric airway pressure at end-expiration. However, NEEP increases airway collapse, alveolar–arterial O₂ difference and dead space, whilst reducing FRC. Thus no longer used.

Negligence.  Civil charge in which the following must be established:

Although the duty of care and failure in that duty may be easy to demonstrate, establishing according to the ‘balance of probabilities’ that harm is a direct result of that failure is usually more difficult. A doctor’s action (or lack thereof) is judged against that of a ‘reasonable’ body of medical opinion, even if that body is a minority (Bolam test); traditionally the fact that such a body of opinion exists has usually been enough for a successful defence against a charge of negligence in the UK. More recently the courts have scrutinised the reasoning and evidence behind such opinion before accepting that it is ‘reasonable’. In the UK, since negligence must be proved in order for compensation to be paid, inability to establish this link will result in no compensation. Thus there have been calls for no-fault compensation schemes similar to that in New Zealand, in which the fact that harm has occurred is enough to result in compensation without having to prove negligence.

[John Hector Bolam, UK shipping assistant and psychiatric patient; suffered fractures in 1954 during electroconvulsive therapy administered without paralysis or restraint, then claimed negligence by the hospital. The claim was dismissed because withholding of anaesthesia was accepted medical practice at the time.]

Neisserial infections.  Mostly caused by two species of the Gram-positive cocci genus:

Neisserial infection is common in complement deficiency.

[Albert Neisser (1855–1916), German physician]

Neomycin sulphate.  Aminoglycoside and antibacterial drug, used orally for selective decontamination of the digestive tract, specifically in hepatic failure and before bowel surgery. Also used topically for skin or mucous membrane infections.

Neonatal resuscitation,  see Cardiopulmonary resuscitation, neonatal

Neonatal Resuscitation Program (NRP).  Programme of training in neonatal CPR, established in 1988 in the USA and administered by the American Heart Association and American Academy of Pediatrics. Similar in concept to the ATLS and related courses. Has been referred to as ‘NALS’ (Neonatal Advanced Life Support), but the term is not an official one.

Neonate.  Child within 28 days of birth. Normally weighs 3–4 kg, with body surface area approximately 0.19 m².

Anatomical and physiological features and principles of anaesthesia are as for paediatric anaesthesia. Perioperative risks are higher than for older children, especially in premature neonates; surgery is usually deferred if possible.

See also, Cardiopulmonary resuscitation, neonatal; Fetal haemoglobin; Fetal monitoring; Neurobehavioural testing of neonates; Obstetric analgesia and anaesthesia; Paediatric advanced life support; Paediatric intensive care; Surfactant

Neostigmine methylsulphate/bromide.  Acetylcholinesterase inhibitor, first synthesised in 1931. Used to increase acetylcholine concentrations at the neuromuscular junction, e.g. reversal of non-depolarising neuromuscular blockade and myasthenia gravis. Also has a direct stimulatory effect on skeletal muscle acetylcholine receptors; in addition, it is thought to have significant presynaptic action, increasing the amount of acetylcholine released. May cause depolarising neuromuscular blockade in overdosage. Other effects are those of muscarinic stimulation, e.g. bradycardia, increased GIT motility and bladder contractility, sweating, salivation, miosis, bronchospasm. Has been used to treat urinary retention and ileus, e.g. postoperatively. Effects on autonomic ganglia are small, consisting of stimulation at low doses and depression at high doses. A quaternary ammonium compound, it crosses the blood–brain barrier poorly and has few CNS effects. Routinely given with atropine or glycopyrronium when administered iv to prevent muscarinic side effects. Active within 1 min of iv injection, with action lasting 20–30 min. Active for up to 4 h after oral administration. Excreted mainly renally, mostly unchanged. Elimination half-life is 50–90 min. May be administered parenterally (as methylsulphate) or orally (as bromide). Has also been given intrathecally; produces analgesia but with increased nausea and vomiting.

Neosynephrine,  see phenylephrine

Nephritic syndrome.  Acute glomerulonephritis characterised by reduction of glomerular filtration rate, haematuria, proteinuria, salt and water retention, increased intravascular volume and hypertension. Most commonly a post-infectious condition, it is also seen in SLE. Usually mild; severe cases may result in acute kidney injury. Distinction between it and nephrotic syndrome has been overplayed in the past and both share common aetiologies.

Nephron.  Basic renal unit; each kidney contains about 1.3 million.

[Sir William P Bowman (1816–1892), English surgeon; Friedrich GJ Henle (1809–1885), German anatomist]

See also, Acid–base balance; Clearance; Diuretics; Renin/angiotensin system

Nephrotic syndrome.  Defined by daily urinary protein excretion exceeding 3.5 g/1.73 m² body surface area. May be caused by primary or secondary (e.g. to diabetes mellitus, pre-eclampsia, connective tissue disease, post-viral hepatitis or streptococcal infection, drugs such as NSAIDs or captopril) glomerular disease. Features include generalised oedema, susceptibility to infection and thromboembolism (especially renal vein thrombosis and DVT) and hyperlipidaemia. Hypoalbuminaemia may lead to altered drug binding.

Treatment includes a low-sodium diet and diuretic therapy to reduce oedema, and a low-protein diet and angiotensin converting enzyme inhibitors to reduce proteinuria. Other treatment is directed against the cause, e.g. corticosteroids in glomerulonephritis.

See also, Renal failure

Nernst equation.  Equation for calculating the membrane potential at which an individual ion is at equilibrium across the membrane (assuming complete permeability to that ion). For ion X:

where E = equilibrium potential

R = universal gas constant

T = absolute temperature

F = Faraday constant (coulombs per mole of charge)

Z = valence of the ion

[X]_o = extracellular concentration of X

[X]_i = intracellular concentration of X.

For chloride, potassium and sodium, E = −70 mV, −94 mV and +60 mV respectively. Since the normal resting membrane potential is about −70 mV, other factors must affect potassium and especially sodium distribution (e.g. relative permeability and the sodium/potassium pump).

[Hermann W Nernst (1864–1941), German physicist; Michael Faraday (1791–1867), English scientist]

See also, Goldman constant field equation

Nerve.  Excitable tissue whose function is the transmission of nerve impulses. Typical peripheral nerves consist of several groups of fascicles. Each fascicle is surrounded by the perineurium and contains a group of neurones, the axons of which are encased in the endoneurium (Fig. 115).

Peripheral nerves originate in the spinal cord, and may be sensory, motor or mixed. Some also carry autonomic nervous system fibres.

See also, Motor pathways; Sensory pathways

Nerve conduction.  Passage of an action potential along neurones; involves waves of depolarisation and repolarisation that move longitudinally across the nerve membrane.

In unmyelinated nerves, impulses spread at up to 2 m/s. Positive charge flows into the depolarised area from the membrane just distally, altering the distal permeability to ions (especially sodium and potassium) as for action potential generation. When the threshold potential is reached, depolarisation occurs. Retrograde conduction is prevented by the refractory period of the membrane proximally.

The myelin sheath of myelinated nerves acts as an insulator that prevents the flow of ions across the nerve membrane. Breaks in the myelin (nodes of Ranvier), approximately 1 mm apart, allow ions to flow freely between the neurone and the ECF at these points. Depolarisation ‘jumps’ from node to node (saltatory conduction), a process that increases conduction velocity (up to 120 m/s) and conserves energy.

[Louis A Ranvier (1835–1922), French pathologist and physician]

Nerve growth factor (NGF).  Protein produced by many cell types; taken up by small sensory and sympathetic nerve fibres via specific receptors and retrogradely transported to the cell body. Required for growth and survival of neurones in the fetus and neonate; released from connective tissue and inflammatory cells following tissue injury in response to cytokine stimulation. Causes hyperalgesia via both central and peripheral effects; thus thought to be important in acute and chronic pain states.

Sofroniew MV, Howe CL, Mobley WC (2001). Ann Rev Neurosci; 24: 1217–81

Nerve injury during anaesthesia.  May occur during general, local or regional anaesthesia.

See also, Cranial nerves; Critical illness polyneuropathy

Nerve stimulator,  see Neuromuscular blockade monitoring; Regional anaesthesia; Transcutaneous electrical nerve stimulation

Netilmicin.  Aminoglycoside and antibacterial drug with similar activity to gentamicin but less active against pseudomonas. Less ototoxic than gentamicin.

Neuralgia.  Pain in the distribution of a defined nerve or group of nerves.

Neuritis.  Inflammation of nerve(s).

Neurobehavioural testing of neonates.  Investigation of the effects of obstetric analgesia and anaesthesia on the neonate is difficult because of many variables, e.g. obstetric details, fetal distress, method of delivery, type and route of drugs administered, methods of analysis of data. In many early studies, aortocaval compression was not avoided.

Neurofibromatosis.  Group of neurocutaneous diseases characterised by multiple tumours derived from the neurilemma sheath of cranial and peripheral nerves/nerve roots.

[Friedrich D von Recklinghausen (1833–1910), German pathologist]

Hirsch NP, Murphy A, Radcliffe JJ (2001). Br J Anaesth; 86: 555–64

Neurokinin-1 receptor antagonists.  Antiemetic drugs, acting via inhibition at neurokinin-1 (NK1) receptors present in the GIT and CNS. Aprepitant is currently licensed for nausea and vomiting induced by cancer chemotherapy. Have also been studied in PONV.

Diemunsch P, Joshi GP, Brichant J-F (2009). Br J Anaesth; 103: 7–13

See also, Tachykinins

Neurolepsis,  see Neuroleptanaesthesia and analgesia

Neuroleptanaesthesia and analgesia.  Use of very potent opioid analgesic drugs (e.g. fentanyl and phenoperidine) combined with butyrophenones (e.g. droperidol and haloperidol) to produce a state of reduced motor activity and passivity (neurolepsis). Introduced in 1959. The term neuroleptanaesthesia is usually restricted to the combination of opioid, butyrophenone and N₂O. Characterised by profound analgesia, sedation and antiemesis, with cardiovascular stability (although mild hypotension may occur). Has been used for premedication, sedation and as the sole anaesthetic technique, with/without neuromuscular blocking drugs, for surgical procedures (now rarely employed for the latter use because of prolonged recovery).

See also, Lytic cocktail

Neuroleptic malignant syndrome (NMS).  Rare condition first described in 1960, characterised by altered consciousness, hyperthermia, autonomic dysfunction and muscle rigidity. Usually triggered by drugs (e.g. butyrophenones, phenothiazines, metoclopramide, lithium, reserpine), although it has been reported during withdrawal of L-dopa in patients with Parkinson’s disease. The mechanism is thought to involve dopamine receptor blockade in the basal ganglia and hypothalamus. Occurs mostly in young males. Incidence is increased with dehydration, CNS disease and exhaustion.

Differential diagnosis is as for hyperthermia (in particular MH), Parkinson’s disease, catatonia, central anticholinergic syndrome, monoamine oxidase inhibitor reaction and infection, e.g. tetanus. Although similar to MH, NMS is generally considered an entirely separate entity.

Mortality is 20–30%, from renal failure, arrhythmias, PE or aspiration pneumonitis.

Adnet P, Lestovel P, Krivosic-Horber R (2000). Br J Anaesth; 85: 129–35

Neuromuscular blockade monitoring.  Ideally, this should be undertaken whenever non-depolarising neuromuscular blocking drugs are used since residual block is common in the recovery room, even after the use of intermediate-acting drugs such as atracurium and vecuronium. A nerve stimulator is used to stimulate a peripheral nerve via surface or needle electrodes; the muscle response is then assessed.

Fuchs-Buder T, Schreiber JU, Meistelman C (2009). Anaesthesia; 64 (Suppl 1): 82–9

Neuromuscular blocking drugs.  Drugs used to impair neuromuscular transmission and provide skeletal muscle relaxation during anaesthesia or critical care.

Apart from the presence or absence of fasciculation, non-depolarising and depolarising neuromuscular blockade may be distinguished by neuromuscular blockade monitoring.

In general, suxamethonium is used for paralysis of rapid onset and short duration, e.g. to allow rapid tracheal intubation. The slower-acting non-depolarising drugs were traditionally used for prolonged paralysis when rapid intubation was not required, although rocuronium, atracurium and vecuronium have bridged the gap between these drugs and suxamethonium (Table 31).

See also, Interonium distance; Nicotine and nicotinic receptors

Neuromuscular junction.  Synapse between the presynaptic motor neurone and the postsynaptic muscle membrane. On approaching the junction, the axon divides into terminal buttons that invaginate into the muscle fibre. The synaptic cleft is 50–70 nm wide and filled with ECF and a basement membrane containing high concentrations of acetylcholinesterase. The muscle membrane is folded into longitudinal gutters, whose ridges conceal orifices to secondary clefts. The orifices lie opposite the release points for acetylcholine (ACh) (Fig. 117).

Martyn JAJ, Jonsson Fagerlund M, Eriksson LI (2009). Anaesthesia; 64 (Suppl 1): 1–9

See also, Neuromuscular blocking drugs

Neuromuscular transmission.  Stages of transmission:

Naguib M, Flood P, McArdle JJ, Brenner HR (2002). Anesthesiology; 96: 202–31

See also, Synapse

Neurone.  Basic unit of the nervous system. Consists of:

[Camillo Golgi (1843–1926), Italian physician]

See also, Nociception

Neuropathy of critical illness,  see Critical illness polyneuropathy

Neuroradiology.  Most neuroradiological procedures are painless and do not require anaesthetic intervention; sedation or anaesthesia may be required in children, uncooperative or neurologically impaired patients or for prolonged procedures. Principles are as for radiology and neurosurgery.

Schulenburg E, Matta B (2011). Curr Opin Anesthesiol; 24: 426–32

Neurosurgery.  Encompasses procedures involving the cranium, brain, meninges, cranial nerves, spinal cord and vertebral column, and those performed for pain management. Basic principles for intracranial surgery are related to maintenance of normal cerebral perfusion pressure and cerebral blood flow, with avoidance of cerebral ischaemia, cerebral steal and increased ICP. Cerebral protection has been employed.

Dinsmore J (2007). Br J Anaesth; 99: 68–74

See also, Spinal surgery

Neurotransmitters.  Substances secreted from presynaptic nerve endings, which act at the postsynaptic membrane to cause excitatory or inhibitory effects. Act via specific receptors that elicit intracellular effects (e.g. by opening membrane ion channels, activating intracellular enzymes or altering DNA transcription). The same neurotransmitter may be excitatory at one synapse, and inhibitory at another.

In general, acetylcholine and the amino acids are involved with fast point-to-point signalling whereas the polypeptides, amines and nitric oxide have a slower, more diffuse regulatory function. More than one neurotransmitter may be secreted by one neurone, e.g. vasoactive intestinal peptide is often secreted with acetylcholine, and is thought to potentiate the latter’s actions. Amines are often secreted with peptide neurotransmitters.

See also, Neuromuscular junction; Receptor theory; Synaptic transmission

Neutral thermal range,  see Thermoneutral range

New injury severity score,  see Injury severity score

New York Heart Association classification.  Method of assessment of cardiac disease (originally cardiac failure), e.g. in preoperative assessment:

Newton.  Unit of force. 1 N is the force required to accelerate a mass of 1 kg by 1 m/s².

[Sir Isaac Newton (1643–1727), English physicist]

Newtonian fluids,  see Fluids

NGF,  see Nerve growth factor

NIAA,  see National Institute of Academic Anaesthesia

Nicardipine hydrochloride.  Calcium channel blocking drug. Used in the UK for treatment of hypertension and ischaemic heart disease; also available parenterally in the USA for short-term reduction of BP, e.g. perioperatively. IV preparation is incompatible with bicarbonate and Hartmann’s solutions.

NICE,  see National Institute for Health and Clinical Excellence

NiCO.  Commercial non-invasive cardiac output measurement system that employs partial CO₂ rebreathing and the Fick principle to estimate cardiac output. A small rebreathing loop is inserted into the patient’s breathing circuit and intermittently increases the volume of the circuit. Concentration and flow of CO₂ are measured by a sensor placed between the patient and the rebreathing loop. The change in cardiac output is proportional to the ratio of the change in CO₂ elimination and the resulting change in end-expiratory CO₂.

Nicorandil.  Potassium channel activator with a nitrate component, used to prevent and treat angina. Causes arterial and venous vasodilatation. Peak plasma levels occur within 30–60 min of administration. Only slightly protein-bound.

Nicotine.  Toxic alkaloid derived from tobacco, mimics certain actions of acetylcholine, and was used to investigate the physiology of the autonomic nervous system. At low doses, it stimulates postsynaptic nicotinic acetylcholine receptors of the neuromuscular junction, autonomic ganglia and adrenal medulla; at high doses, it blocks them. Also causes CNS stimulation, followed by depression.

Nifedipine.  Dihydropyridine calcium channel blocking drug, affecting coronary and peripheral vascular smooth muscle more than myocardial muscle. Negative inotropic effect is usually insignificant because of baroreceptor-mediated tachycardia.

Has no antiarrhythmic action. Used in hypertension, ischaemic heart disease and Raynaud’s phenomenon. Active within 20–30 min of oral administration, but a faster response follows sublingual retention of the capsule’s contents (though not licensed for sublingual use). May thus be administered sublingually during anaesthesia. 95% protein-bound. Half-life is 3–5 h. Metabolised in the liver and excreted renally.

[Maurice Raynaud (1834–1881), French physician]

Nimodipine.  Dihydropyridine calcium channel blocking drug, preferentially affecting cerebral vascular smooth muscle. Increases cerebral blood flow, especially to poorly perfused areas, e.g. those affected by arterial spasm following subarachnoid haemorrhage (SAH).

Reacts with PVC infusion tubing; polypropylene and polyethylene are suitable. May be degraded by light.

NIPPV,  see Non-invasive positive pressure ventilation

NIRS,  see Near infrared spectroscopy

NISS.  New injury severity score,

see Injury severity score

Nitrazepam.  Benzodiazepine widely used as a hypnotic drug. Has also been used as an anticonvulsant in childhood myoclonic epilepsy. Onset of sleep occurs within an hour; duration of action is 4–8 h. Extensively protein-bound; elimination half-life is up to 30 h, resulting in hangover effects during the day.

Nitric oxide (NO).  Oxide of nitrogen, active as a biological mediator throughout the body but especially in:

Synthesised in endothelial cells during the oxidation of L-arginine to L-citrulline, the reaction being catalysed by NO synthase (NOS). The NO thus produced diffuses into vascular smooth muscle and converts inactive guanylate cyclase into the active form; the latter converts guanosine triphosphate into cyclic guanosine monophosphate, which causes vascular relaxation (Fig. 118). Two forms of NOS exist: the constitutive (endothelial) form, present in vascular and brain tissue, which produces small quantities of NO continuously (eNOS); and the inducible form, present in macrophages (iNOS).

In sepsis, NO production is thought to be increased by endotoxin, the action of cytokines, e.g. tumour necrosis factor and certain interleukins. The amount of the inducible form of NOS increases, resulting in overproduction of NO with resultant excessive vasodilatation. NOS inhibitors have been investigated experimentally in the treatment of sepsis.

In neonatal, paediatric or adult pulmonary hypertension, inhaled NO (1–150 ppm) has been used to produce selective pulmonary vasodilatation without systemic effects. A clear effect on outcome in ARDS has not been conclusively demonstrated.

NO has a biological half-life of < 5 s, its action being terminated by combining with haemoglobin to form methaemoglobin.

Measured in gaseous form using a chemiluminescence reaction (NO + ozone → O₂ + NO₂ + light) or electroanalysis using a specific electrode. Levels in tissues are measured using electron paramagnetic resonance or fluorescence spectroscopy.

Nitrogen.  Non-metallic element existing in the atmosphere as a colourless, odourless ‘inert’ gas (isolated in 1772). Forms 78.03% of atmospheric air. Atomic weight is 14; boiling point is −195°C. Obtained by fractional distillation of air. Reacts poorly with other substances. Blood/gas solubility coefficient is 0.014. Has anaesthetic properties at hyperbaric pressures (see Inert gas narcosis). Converted into organic compounds by nitrifying bacteria and plants, and present throughout the body in amino acids and proteins.

See also, Nitrogen balance; Nitrogen washout

Nitrogen balance.  Difference between the amount of nitrogen ingested (as amino acids or proteins) and the amount of nitrogen excreted (mainly urinary). Usually measured within a 24-h period. Negative if losses exceed intake, e.g. catabolism, starvation; positive if intake exceeds losses, e.g. during recovery from severe illness.

Other losses occur from sweat and faeces (e.g. 2–4 g per l GIT fistula fluid lost per 24 h).

Calculation is a useful guide to appropriate nutrition in critical illness. A normal adult requires about 0.15 g N/kg/day; this may double in severe sepsis.

See also, Energy balance

Nitrogen, higher oxides of.  Nitric oxide (NO), nitrogen dioxide (NO₂) and nitrogen trioxide (N₂O₃); the latter decomposes to form NO and NO₂. NO reacts with O₂, forming NO₂, which dissolves in water to form nitrous and nitric acids. The gases are produced during some fires, during manufacture of N₂O, and in the metal industry. Irritant if inhaled, they cause mild upper airway symptoms initially but pulmonary oedema several hours after initial recovery. Severe pulmonary fibrotic destruction may follow 2–3 weeks later. Formation of nitrates in the body may result in vasodilatation and hypotension, and cause methaemoglobinaemia. Treatment is supportive. Contamination of some N₂O cylinders in 1967 in the UK led to their widespread recall. May be tested for using moistened starch iodide paper, which turns blue on exposure. NO is involved in intercellular communication and control of vascular tone.

See also, Smoke inhalation

Nitrogen narcosis,  see Inert gas narcosis

Nitrogen washout.  Elimination of nitrogen from the lungs whilst breathing non-nitrogen-containing gas. During successive breaths, the concentration of nitrogen exhaled falls as an exponential process, falling to about 2.5% after 7 min in normal patients. During anaesthesia using circle systems, 7–10 min high fresh gas flow is required to remove most body nitrogen. Elimination is prolonged if ventilation is distributed unevenly (see below).

Nitroglycerin,  see Glyceryl trinitrate

Nitroprusside,  see Sodium nitroprusside

Nitrous oxide (N₂O).  Inhalational anaesthetic agent, first isolated by Priestley in 1772. Suggested as being a useful analgesic by Davy in 1799; first used for dental extraction by Wells in 1844 but superseded by diethyl ether. Reintroduced by Colton in 1863.

Manufactured by heating ammonium nitrate to 240°C and removing impurities (e.g. higher oxides of nitrogen, ammonia and nitric acid) by passage through scrubbers and washers. Water vapour is also removed.

Excreted unchanged from the lungs; a small amount diffuses through the skin.

Commonly used for analgesia (above 20%) and as a carrier gas for other inhalational agents and O₂, usually in concentrations of 50–66%. Although weakly anaesthetic and rarely adequate alone, it reduces the requirement for other agents. Its adverse effects and concern about its effects on the environment have led to a reduction in its use and replacement by air. Recent evidence suggests an increased incidence of major cardiovascular and respiratory complications after major surgery if N₂O is used, though the findings are controversial and may be related to differences in F_IO₂ rather than to N₂O itself.

Also used in the cryoprobe.

See also, Environmental safety of anaesthetists; Nitrogen, higher oxides of; Pollution; Relative analgesia

NIV.  Non-invasive ventilation,

see Nasal positive pressure ventilation

Nizatidine.  H₂ receptor antagonist used in peptic ulcer disease; similar to cimetidine but does not cause enzyme inhibition. Well absorbed orally, it is 40% protein-bound, with 90% excreted by the kidneys.

NMDA receptors,  see N-Methyl-D-aspartate receptors

NMJ,  see Neuromuscular junction

NMR.  Nuclear magnetic resonance,

see Magnetic resonance imaging

NO,  see Nitric oxide

No reflow phenomenon.  Reduction in organ blood flow following a period of ischaemia or infarction, without mechanical vessel obstruction. Has been observed affecting the heart and brain, e.g. after MI/myocardial ischaemia and CVA/cerebral ischaemia respectively. The aetiology is unclear but small vessel vasospasm, endothelial oedema or extrinsic compression by tissue oedema, increased blood viscosity, platelet aggregation and venous congestion have all been suggested. Treatment has been aimed at all these factors, with varying degrees of success.

Rezkalla SH, Kloner RA (2002). Circulation; 105: 656–62

Nociceptin,  see Orphanin FQ

Nociception.  Sensation of noxious stimuli, i.e. associated with injury or threatened injury.

Other types may also exist. Although initially described and most abundant in skin, they also exist in other tissues, e.g. muscle, joints, teeth. Injury increases their response and sensitivity.

See also, Pain; Pain pathways

Nodal arrhythmias,  see Junctional arrhythmias

Non-depolarising neuromuscular blockade.  Caused by competitive antagonism of acetylcholine (ACh) by non-depolarising neuromuscular blocking drugs at the ACh receptors of the neuromuscular junction. The end-plate potential produced by ACh diminishes as receptor occupancy by the neuromuscular blocking drug increases; when it fails to reach the threshold for depolarisation, neuromuscular transmission fails. This only occurs when >80–90% of ACh receptors are blocked, demonstrating the wide margin of safety of neuromuscular transmission.

Blockade may also be potentiated by excess drug at the neuromuscular junction, e.g. caused by overdose, or reduced metabolism, excretion or muscle blood flow.

See also, Neuromuscular blockade monitoring; Priming principle

Non-invasive positive pressure ventilation.  An alternative to IPPV via tracheal tube, positive pressure ventilation may be applied via a tightly fitting nasal mask, facial mask, nasal ‘pillows’ that fit into the nostrils, or a ‘helmet’ that encloses the whole head. Ventilators may deliver a set volume or, more commonly, a set pressure. Uses include: ventilatory support in acute respiratory failure (especially exacerbations of COPD and cardiogenic pulmonary oedema); facilitation of extubation/weaning from ventilators; support for patients requiring nocturnal IPPV (e.g. central sleep apnoea, neuromuscular disorders); and palliation in end-stage respiratory disease.

BIPAP (bi-level positive airway pressure) refers to a technique in which two levels of positive pressure are provided during inspiration and expiration. Airflow in the patient circuit is sensed by a transducer and augmented with a preset level of positive pressure. Cycling between inspiratory and expiratory modes may be triggered by the patient’s spontaneous breaths or according to a preset rate (cycling either fully automatically or only if the patient fails to take a spontaneous breath within a certain time period). CPAP may also be delivered in either mode. BIPAP may also be administered via an oral mask.

Disadvantages and complications include discomfort, gastric distension, vomiting and aspiration of gastric contents, and pressure necrosis, e.g. to the bridge of the nose.

Nava S, Hill N (2009). Lancet; 374: 250–9

Non-parametric tests,  see Data; Statistical tests

Non-rebreathing valves.  Prevent exhaled gas from passing upstream from the patient in anaesthetic breathing systems, thus almost eliminating rebreathing (but reducing efficiency because dead space gas is wasted). Most commonly used in draw-over techniques and for CPR with self-inflating bags. Also used in demand valves. For use with a fixed fresh gas supply, a reservoir bag is required unless fresh gas flow rate exceeds peak inspiratory flow rate. Should be placed as near to the patient as possible, e.g. attached directly to the facemask/tracheal tube.

Malfunction (e.g. due to condensation of water vapour) may cause sticking of the valve or rebreathing. Barotrauma may occur if high internal pressure holds the expiratory port closed, e.g. during apnoea with high fresh gas flow.

[Ambu: from ambulant, Danish for movable; Asmund S Laerdal (1913–1981), Norwegian businessman and manufacturer; Henning M Ruben (1914–2004), Danish anaesthetist]

Non-steroidal anti-inflammatory drugs (NSAIDs).  Group of chemically dissimilar compounds with anti-inflammatory, antipyretic and analgesic actions. Widely used for mild pain (e.g. musculoskeletal disease, headache, dysmenorrhoea), inflammatory disorders (especially musculoskeletal) and postoperative analgesia. Individual responses to NSAIDs are variable and many drugs may have to be tried before achieving optimal benefit.

Effects are via inhibition of cyclo-oxygenase, resulting in reduced prostaglandin, prostacyclin and thromboxane production (see Fig. 15; Arachidonic acid). Inhibitors of cyclo-oxygenase-2 (COX-2) (e.g. parecoxib, celecoxib) have been produced for their relative lack of GIT side effects.

Evidence suggests that NSAIDs reduce opioid requirements when used intra-/postoperatively. Should be used cautiously if there is a risk of increased perioperative bleeding or renal impairment (the latter, for instance, in the elderly, diabetics, and after cardiac, hepatobiliary, renal or major vascular surgery) or sensitivity to aspirin. Postoperative renal dysfunction and GIT ulceration/bleeding should lead to cessation of therapy.

Noradrenaline (Norepinephrine).  Catecholamine, the immediate precursor of adrenaline (differing by one methyl group on the terminal amine). A neurotransmitter in the sympathetic nervous system, ascending reticular activating system and hypothalamus. Also a hormone, forming about 20% of the catecholamines released from the adrenal medulla.

Predominantly stimulates α-adrenergic receptors (non-selectively), although with some β₁-receptor stimulation. After secretion, 80% is taken up by postganglionic sympathetic nerve endings for reuse (uptake₁); the remainder is metabolised by catechol-O-methyltransferase and monoamine oxidase or taken up by other cells, e.g. vascular smooth muscle (uptake₂).

Used as an inotropic drug when SVR is low, e.g. in sepsis. An extremely potent vasopressor drug, it increases both systolic and diastolic arterial BP via arterial and venous vasoconstriction. There may be compensatory bradycardia caused by baroreceptor reflex activation. Coronary perfusion is increased but with increased myocardial O₂ demand. Cardiac output may increase or decrease depending on clinical circumstances. Cerebral blood flow and O₂ demand may fall. Although hypotension may be corrected, renal and mesenteric vasoconstriction may reduce renal blood flow.

Supplied commercially as noradrenaline tartrate.

Tachyphylaxis may occur. Tissue necrosis may follow extravasation.

Norepinephrine,  see Noradrenaline

Normal distribution,  see Statistical frequency distributions

Normal solution.  One containing 1 gram equivalent weight of substance per litre. So-called ‘normal’ saline solution (0.9%) is incorrectly described, being less than 1/6 normal.

See also, Equivalence

Noscapine,  see Papaveretum

Nose.  Entrance to the pharynx and thence larynx and lungs. Apart from its olfactory role, it filters, humidifies and warms inspired air with its extensive vascular surfaces (turbinates and septum). Filtering relies on the mucous lining which traps particles larger than 4–6 µm, sweeping them back to the pharynx. Sneezing also rids the nose of irritants.

Trauma to the nose may result from passage of a tracheal or nasogastric tube, or nasal airway. Resultant epistaxis may be severe, and may be reduced by prior administration of cocaine spray or paste, or other vasopressor solutions, e.g. xylometazoline 0.1%.

Maxillary and ophthalmic nerve blocks may be used for operations on or around the nose.

[Arthur J Moffett (1904–1995), Birmingham otolaryngologist]

See also, Choanal atresia; Ear, nose and throat surgery

Nosocomial infection.  Infection acquired as a result of a patient’s admission to hospital. Occurs in up to 10% of patients, with mortality of up to 5%. More common in the acutely ill (e.g. on ICU).

Sites of infection in order of decreasing frequency: urinary tract infection, surgical wound infection, nosocomial pneumonia and bacteraemia. Organisms most commonly involved in order of decreasing frequency: Staphylococcus aureus, pseudomonas, coagulase-negative staphylococci, candida species and Escherichia coli. Fungal infection is especially common in immunosuppressed patients.

Vincent JL (2003). Lancet; 361: 2068–77

See also, Ventilator-associated pneumonia

Nosocomial pneumonia.  Hospital-acquired chest infection occurring > 48 h after hospital admission; excludes infections incubating on admission. May occur in up to 25% of ICU patients and increases hospital mortality, length of stay and costs.

Often more than one organism is involved.

Approaches to clinical diagnosis vary but criteria include new, progressive or persistent CXR abnormalities, with evidence of infection (e.g. purulent sputum, hypo- or hyperthermia, and a low [< 5000/mm³] or raised [> 10 000/mm³] white cell count). Isolation of the responsible organism(s) is best undertaken using bronchoalveolar lavage, either blind or via fibreoptic bronchoscopy. Therapy should be organism-specific when possible, but broad-spectrum antibiotics are frequently necessary until the organism is identified.

Torres A, Ferrer M, Badia JR (2010). Clin Infect Dis; 51 Suppl 1:S48–53

See also Infection control; Nosocomial infection; Sepsis; Ventilator-associated pneumonia

Notifiable diseases.  Diseases that an attending doctor is required by law to report to the local authority proper officers, usually via the consultant in communicable disease or chief environmental health officer. The scheme allows epidemiological surveillance and early identification of potential epidemics (Table 32). Failure to send details of the case on a certificate may result in conviction and a fine.

Novoseven,  see Eptacog alfa

NPSA,  see National Patient Safety Agency

NRP,  see Neonatal Resuscitation Program

NSAIDs,  see Non-steroidal anti-inflammatory drugs

NSTEACS.  non-S–T segment elevation acute coronary syndromes, see Acute coronary syndromes

NSTEMI.  non-S–T segment elevation myocardial infarction, see Acute coronary syndromes; Myocardial infarction

Nuclear cardiology.  Assessment of cardiac function using gamma cameras to trace radioisotopes. Technetium-99m-labelled blood may be followed through the heart during first pass of a bolus, or over many cardiac cycles linked to the ECG (multigated acquisition imaging; MUGA). Individual chamber movement and valve function may be observed, and ejection fraction calculated by recording the number of counts in systole and diastole. Alternatively, the uptake of thallium-201 by cardiac tissue may be observed (uptake by normal myocardium is proportional to blood flow). Thallium scanning may be enhanced by giving intravenous dipyridamole to precipitate ischaemia by causing coronary steal. Recently infarcted myocardium may be labelled with technetium-99m pyrophosphate. Other tracers used to identify areas of infarction, necrosis or inflammation include indium-111, gallium-67 citrate, and radiolabelled myosin-specific antibodies.

Nuclear magnetic resonance,  see Magnetic resonance imaging

Null hypothesis.  In statistics, the assumption that the observed frequency of an event equals the expected frequency. It may state that any observations are due to chance alone, or that the groups studied come from the same population; statistical tests aid the acceptance or rejection of this hypothesis (and whether an alternative hypothesis, e.g. that observed differences are caused by treatment, can be accepted). In traditional ‘hypothesis testing’, results are expressed in terms of the probability that the null hypothesis is true for the case concerned.

See also, Confidence intervals; Statistical significance

Number needed to treat (NNT).  Indicator of treatment effect in clinical trials. The inverse of absolute risk reduction, it gives the number of patients that need to be treated in order to prevent a specified undesirable outcome (e.g. PONV). For example, for an antiemetic with NNT for PONV of 5, one needs to treat five patients with the drug in order to prevent one patient suffering PONV. Combines both the efficacy of the drug and the incidence of the condition treated; for example, an antiemetic that is effective in 100% of patients will have a NNT of 5 if the incidence of PONV is 1:5, but if it is only 50% effective (or the incidence of PONV falls to 1:10) the NNT will be 10. Number needed to harm (NNH) is a similar concept, indicating the number of patients needed to receive a drug before one suffers a complication.

See also, Meta-analysis; Odds ratio; Relative risk reduction

Nurses, prescription of drugs by.  In the UK, specially trained nurses have been able to prescribe from a limited formulary since 1998; from 2006, regulations allowed certain nurses (and pharmacists) to prescribe any licensed drug (including opioids) so long as it is within their specific competence and local clinical governance frameworks. Other nurses and pharmacists are able to prescribe within specific management plans drawn up by a doctor for individual cases. Likely to have most relevance to acute and chronic pain management, premedication and intensive care.

See also, Midwives, prescription of drugs by

Nutrition.  An adequately balanced daily supply of carbohydrates, fats, proteins, vitamins, electrolytes, trace elements and water is essential to maintain normal health.

Energy requirements depend on the particular circumstances for each individual, e.g. they increase after trauma and burns (see Catabolism), and with pyrexia (by about 10% for every °C above normal). Patients should be fed via the oral route if possible, preferably with normal food.

For critically ill patients, more precise estimation of energy balance is necessary, whatever the route of administration. Once energy requirements have been determined, it is divided into carbohydrate (4 Cal/g) and fat (9 Cal/g) components to accompany nitrogen (150–200 Cal/g nitrogen). Carbohydrate should comprise 40–50% of energy requirements. Appropriate enteral or parenteral solutions are then selected from commercially available products (some pharmacies make up their own solutions), satisfying requirements for energy, fluid and electrolytes. Vitamins may be added as required.

Bistrian BR, McCowen KC (2006). Crit Care Med; 34: 1525–31

See also, Malnutrition; Metabolism; Nitrogen balance; Nutrition, enteral; Nutrition, total parenteral

Nutrition, enteral.  Feeding via the GIT. Ideal route is by mouth using normal or liquidised food and calorific/protein supplements, if necessary. Commonly performed via fine-bore nasogastric tubes on ICU. Alternatives include a nasojejunal feeding tube (using a weighted tube or passed via endoscopy), percutaneous endoscopic gastrostomy or a jejunostomy tube placed at the time of surgery.

In patients with adequate GIT function, it is preferable to TPN as it is more physiological, provides protection against stress ulcers, maintains intestinal barrier integrity (thus reducing bacterial translocation) and promotes biliary flow, preventing the cholestasis commonly seen with TPN.

Principles are those of nutrition generally. Carbohydrate is the usual energy source in most enteral feeds, but high concentrations increase osmolality, causing diarrhoea. The protein source is usually whole protein, although preparations containing oligopeptides or amino acids are useful in pancreatic disease and malabsorption syndromes. Medium chain triglycerides are the usual source of fat. Most feeds also contain fibre.

Zaloga GP (2006). Lancet; 367: 1101–11

See also, Energy balance; Nutrition, total parenteral

Nutrition, total parenteral (TPN).  Administration of total nutritional requirements by iv infusion; it may be required in patients who are hypercatabolic and/or have an abnormal GIT. Commonly required in critically ill patients on ICU with abdominal pathology or multiorgan failure. Only indicated if enteral nutrition fails to deliver requirements or is impossible to use. May also be used to support enteral nutrition.

Principles are those of nutrition generally, i.e. calculation of nitrogen balance, energy and fluid requirements. Nitrogen and the energy source should be given together, preferably continuously. 5–6 mmol potassium and 1–2 mmol magnesium are required per gram of nitrogen.

The nitrogen component is given as mixtures of essential and non-essential amino acids (the nitrogen content varies considerably between different solutions). Some amino acid solutions contain electrolytes and most are hypertonic. Some contain energy sources, e.g. glucose and fructose. Carbohydrate is usually given as glucose 10–50%, and requires central venous infusion to avoid venous thrombosis. Other energy sources have also been used, e.g. sorbitol, xylitol and ethanol. Insulin is usually required to control hyperglycaemia associated with glucose-rich infusions. ‘Tight’ glycaemic control is no longer recommended as it is associated with greater morbidity secondary to hypoglycaemia. Fat is usually administered as 10 or 20% soya bean oil emulsions; allergic reactions may occur rarely with the 20% preparation. Trace elements and vitamins must be added.

Most solutions are administered from one large bag via a pump and a single dedicated central venous cannula, although a peripheral line is acceptable for temporary infusion of fat emulsion.

The patient should be encouraged to mobilise to prevent muscle breakdown.

Blackburn GL, Wollner S, Bistrian BR (2010). Arch Surg; 145: 533–8

See also, Energy balance; Nutrition, enteral

Nystatin.  Polyene antifungal drug, principally used for treatment of Candida albicans infections of skin, mucous membranes and GIT. Not absorbed when administered by mouth and too toxic for parenteral use. Available as tablets, oral suspension, cream or pessaries.