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 Withdrawn from the UK market in 2003.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