37 Practical anaesthesia

Andrew Foo

Latex allergy 1010

Herbal medicines and anaesthesia 1014

Anne Rossiter

Blood exposure incidents 1016

Anne Troy

Target-controlled infusions 1020

Babinder Sandhar

Death on the table 1024

Dealing with a complaint 1026

Rhys Thomas, Rob Dawes, Simon Mercer, and S. Jagdish

Military anaesthesia 1029

Damage control resuscitation (DCR) 1030

Medical Emergency Response Team (MERT) 1032

Drawover anaesthesia: the triservice anaesthetic apparatus (TSAA) 1034

Total intravenous anaesthesia: military uses 1036

Andrew Bodenham

Long-term venous access 1040

Alex Grice

Oesophageal Doppler monitoring 1046

Robert Sneyd

Depth of anaesthesia monitoring 1050

John Carlisle

Cardiopulmonary exercise testing (CPET) 1053

John Saddler

Neuromuscular blockers: reversal and monitoring 1054

Pete Ford

Thromboelastography 1060

Report UK suspected anaphylactic reactions at http://www.aagbi.org/anaphylaxisdatabase.htm.

Adverse pharmacological effect related to genetic status, e.g. angio-oedema.

Machine or operator error.

Vasovagal episode.

Pseudoallergic or anaphylactoid reactions—direct histamine release by active agent or indirect release by complement activation.

The quarternary ammonium group found in NMBD is widely present in other drugs, foods, cosmetics, and hair care products. Previous sensitisation is possible, predominantly in females.

If previous penicillin anaphylaxis, neither cephalosporins nor imipenem should be used.

Incidence of cross-reactivity to newer cephalosporins in patients with penicillin allergy is uncertain as cross-reactivity is often incomplete. Cephalosporins can be given to most patients who declare themselves as ‘penicillin allergic’—give slowly and incrementally in case of anaphylactoid (dose-related) response.

Timing is important. Onset is usually rapid following IV drug bolus. Slower onset is expected if, for example, gelatin infusion, latex sensitivity, or diclofenac suppository responsible.

Cardiovascular collapse has been reported in 88% of cases, bronchospasm in 36%, and angio-oedema in 24% of AADR, with cutaneous signs in ∼50%.

Basal plasma tryptase concentration is usually <1ng/ml. Levels up to 15ng/ml are seen in pseudoallergy, i.e. non-specific, anaphylactoid reactions, and non-life-threatening anaphylaxis. Higher values are more likely to indicate IgE mediation.

Currently only helpful in confirming penicillin, suxamethonium, and latex allergy. Sensitivity low—negative result still requires skin testing.

Tests should take place at 4–6wk post-event to allow regeneration of IgE.

Antihistamines should not have been given within the last 5d.

SPT are used initially. Some drugs, e.g. atracurium and suxamethonium, can produce a false positive result with IDT.

Testing is required to all drugs given before the event. Remember antibiotics, latex, chlorhexidine, and lidocaine, if mixed with propofol.

Suspected local anaesthetic allergy is best tested by challenge as recommended by Fisher.¹

Negative control is with saline (to exclude dermographia). Positive control is with commercially available histamine solution. The latter demonstrates normal skin response. Weal and flare gives a reference for reactions to test drugs.

Weal >2mm wider than saline control is interpreted as positive. Positive test with undiluted drug is repeated with 1:10 dilution to reduce chance of false positive.

Following a positive result, other drugs in the same pharmacological group are tested. In NMBD allergy, up to 60% of people may be sensitive to other relaxants.

If there is a strong history but negative SPT, diluted drugs can be tested by IDT.

In the absence of positive skin testing, best advice is given based on the clinical history.

Ensure hospital notes are marked. Inform general practitioner.

Report reaction to the Medicines and Healthcare Products Regulatory Agency (‘yellow card system’). AADR is currently underreported.

Do not use IV ‘test’ doses—unsafe if true allergy exists.

If any doubt about induction agents use inhalational induction. There are no reports of anaphylaxis to inhalational anaesthetics.

If NMBD reaction give relaxant-free anaesthetic if possible. In a long-term follow-up of patients with severe reactions to NMBD 3 of 40 subsequent anaesthetics using muscle relaxants produced probable anaphylactic reactions.²

If NMBD must be used, ideally test to your chosen drug by SPT preoperatively.

In proven NMBD allergy, give chlorphenamine (10mg IV) and hydrocortisone (100mg IV) 1hr preinduction.

Contact dermatitis: a type IV (delayed) hypersensitivity reaction based on allergic sensitisation mediated by T lymphocytes. Presents over 48–72hr with an eczematous eruption. This can progress to lichenification and scaling on chronic exposure.

Type I hypersensitivity: development of latex sensitivity is dependent on previous exposure. IgE-mediated type I hypersensitivity has been attributed to the Hev b proteins in latex. The three main presentations are:

Neural tube defects (including spina bifida): incidence of latex sensitivity due to recurrent bladder catheterisation is 20–65%.

Associated medical conditions: patients with atopy, asthma, rhinitis, and severe dermatitis have an increased incidence of sensitivity.³

Healthcare workers: prevalence of sensitivity can be between 3 and 12%.¹

Occupation: rubber industry workers, occupations involving the use of protective equipment (policemen, hairdressers, service food workers).

Fruit allergens: patients allergic to fruit have an 11% risk of a latex reaction. Cross-reactivity has been demonstrated with certain fruit allergens (banana, chestnut, avocado, passion fruit, tomato, grape, celery, peach, water melon, cherry, and kiwi fruit).¹

Patients with a positive clinical history may be referred for testing before surgery. This may not be possible in an emergency. Current tests have a sensitivity of 75–90%. This includes a blood test specifically for latex-specific IgE or a skin prick test (performed by trained staff).⁴ If these tests are unclear or negative despite a clear history, consider other tests such as provocation testing and patch testing to be performed by a specialist.

The operating theatre should be prepared the night before and the patient should be scheduled first on the list. This reduces the number of latex particles in the air.

‘Latex allergy’ notices should be placed on the anaesthetic and theatre doors.

Only use latex-free equipment within the anaesthetic and surgical areas. Each theatre suit should have a list detailing which equipment is guaranteed latex free. LMA (Intravent), most ETT, and airways are latex-free.

Remove non-essential equipment from the vicinity of the patient.

Limit staff traffic during surgery.

Resuscitation equipment must be latex free.

Prophylactic use of antihistamines and corticosteroids has not been established.

Follow latex allergy precautions on the ward and in theatre. This should include a latex-free trolley containing the following latex-free equipment: gloves (synthetic rubber), masks and airways (plastics), endotracheal tubes (PVC), reservoir bags (neoprene), valves (silicone), IV tubing, IV cannulae (Teflon), syringes, bellows, circuits. There should also be barrier protectors for placement between latex-containing items and the patient's skin (e.g. Webril).

Measures should be in place to avoid latex sensitisation with hospital staff.

Of these, 70% do not disclose this fact to their doctor.

Content and concentrations of herbal remedies may vary dramatically.

Most herbal remedies are harmless, but some may have important consequences for anaesthesia.

Contact with broken or damaged skin, e.g. cuts, abrasions, and eczema.

Splashes to mucous membranes such as the mouth or eye.

Large-bore hollow needles.

High viral load of the source patient (donor).

Injury from a needle that has been in an artery or vein.

Follow universal precautions but, particularly, do not resheath needles and do dispose of your own clinical waste.

Encourage bleeding of puncture wound.

If splash to eye or mouth irrigate with water/saline.

Follow your hospital's policy and procedure for blood exposure incidents.

Complete incident form—important to record the event in case of health problems developing later.

Consider whether your injury has led to the patient involved or anyone else being exposed to your blood. This is more likely if your injury has occurred during an interventional procedure.

The assessment will consider:

The OHS will liaise with the source patient's clinical team to obtain consent for testing for BBVs. Most units test routinely for all three BBVs providing consent is given to do so.

This should be done as a matter of urgency if the source patient is suspected of having HIV infection.

If consent cannot be obtained a risk assessment of the source patient's status will be required to determine the need for post exposure prophylaxis.

If consent is withheld or delays are likely post exposure prophylaxis may be commenced based on the risk assessment.

Follow-up serology at 6, 12, and 24wk identifies early disease and allows active management. No practice restrictions are required during this period unless seroconversion occurs.

HBV—depending on immunisation status, victims will receive HBV vaccine alone or in combination with HBV immunoglobulin. Treatment should begin within 48hr of injury.

HIV—ideally PEP should commence within 1hr but may be given up to 1wk following injury. Currently a combination of antiretroviral agents is recommended for 4wk. Up-to-date advice on drug selection can be obtained from the UK's Department of Health or Health Protection Agency websites (www.dh.gov.uk or www.hpa.org.uk) The protocol may require alteration if the source patient is not treatment naïıve. PEP can produce unpleasant side effects as it is toxic to the liver, kidneys, and bone marrow, and their function is monitored during treatment. A significant proportion of injured HCWs discontinue treatment because of side effects.

HCV—no PEP is recommended. Early treatment of acute disease with alpha interferon ± ribavirin has been shown to be successful in reducing the risk of long-term chronic liver disease.

Check to see if testing has been carried out as part of clinical assessment.

Obtain informed consent for testing for BBVs.

If consent unavailable obtain clinical/social history to assess risk factors for possible infection (see below).

If exposure to BBV is likely contact on-call microbiologist, consultant in communicable disease control, or genito-urinary medicine specialist.

Co-operate with obtaining consent from source patient for testing for BBVs. This will usually mean ensuring the patient has recovered sufficiently from an anaesthetic to give informed consent.

In the UK there are GMC guidelines concerning testing without informed consent in situations where the patient is anaesthetised, unconscious, or has died. Testing can only be supported if the test is likely to be in the immediate clinical interests of the patient.

PEP may be started as a result of a risk assessment of the injury whilst awaiting recovery from anaesthesia/sedation, etc.

Consent discussion should cover:

If consent is not available participate in risk assessment of source patient status.

History consistent with increased risk of infection with BBVs includes:

Occupational health advice must be sought on the range of activities that can be undertaken by infected doctors.

Currently participation in EPPs is barred for doctors in the UK who are:

Most clinical procedures carried out by anaesthetists do not fall within the definition of EPP. Procedures that may be exposure prone, depending on the technique used, include the placement of portacaths and insertion of chest drains in trauma cases where there may be multiple rib fractures.

Mouth to mouth resuscitation can be undertaken by an EPP-restricted worker if no competent non-restricted colleague is available as the benefit to the patient greatly outweighs the small risk of BBV transmission in these circumstances.

Drug is then distributed to compartments V₂ and V₃. The movement of drug between the compartments is governed by intercompartmental rate constants (e.g. K_eo for brain/effect site concentration).

Once infusion is stopped this bias is close to zero.

Because pharmacodynamic variation is much greater than pharmacokinetic variation the target concentration must be titrated to achieve the required effect in any individual patient.

Elderly patients have a small volume of distribution with increased sensitivity to drugs. Doses, therefore, should be titrated in small steps.

Children require a different set of pharmacokinetic variables for propofol, which have been incorporated into the Paedfusor and Alaris Asena PK system.

Benzodiazepine premedication, nitrous oxide, and opioids all reduce propofol requirements.

Allow time for the effect-site concentration to increase towards the target blood concentration. Oxygen should be administered during the induction phase to ensure an adequate SpO₂.

Increase the target concentration to achieve the desired level of anaesthesia for the procedure, the individual patient, and the balance of other agents such as analgesics.

Wait to allow for the effect-site concentration to rise towards the target concentration.

Reduce the target value as propofol continues to be redistributed.

Wait to allow for the effect-site concentration to rise.

Increase the target in small steps (0.5–1µg/ml) until the desired effect is achieved.

Titrate to effect.

The majority of patients will wake at 1–2µg/ml.

When patients are breathing spontaneously, respiratory rate and ETCO₂ are good indicators as to adequacy of anaesthesia.

The use of moderate doses of opioid analgesics, for example, remifentanil or nitrous oxide, will allow a lower target concentration of propofol to be used—up to one third.

As open TCI systems allow the use of different drugs and drug concentrations, vigilance is needed to ensure that the correct drug and concentration are used.

The models used in the available TCI systems calculate dose requirements in obese patients differently. This may result in over-/under estimating the amount of drug required. There is little available evidence regarding the use of TCI in morbidly obese patients, and many anaesthetists input values between ideal body weight and total body weight and then titrate to response.¹

If drug and IV fluids are connected to the same cannula by means of a T-piece or three-way tap:

Coadministration of drugs by the same giving set is not ideal as a change in the rate of one infusion can affect the other, especially if there is a significant dead-space after the common connection or T-piece.

The most reliable method is to use a separate, dedicated access site.

1–2ml 1% lidoocaine can be injected through the cannula prior to induction to avoid discomfort from propofol at the start of the infusion.

Beneficial in laryngoscopy/bronchoscopy where delivery of an inhaled agent may be difficult, and in thoracic surgery, where it does not appear to inhibit the hypoxic vasoconstrictor reflex.

Safe to use in patients with a history of malignant hyperthermia.

Recovery with minimal ‘hangover’.

Inability to monitor drug concentration.

Slow recovery following long operations unless the dose of propofol is decreased by combination with remifentanil.

Interruption to the delivery of propofol may take longer to recognise.

Dealing with the relatives—break the news to the relatives in a sympathetic and considerate way. This should be done by a team of senior staff (surgeon, anaesthetist, and nurse). Interpreters, chaplain, or social workers may be indicated in specific circumstances. It is highly inadvisable to let the surgeon or any single consultant see the relatives alone, as misunderstandings can occur. The initial interview should convey brief facts about the case to allow the relatives to take in the bad news. A nurse or carer should stay with the family to comfort them and offer practical help as required. After a suitable interval, the team should return and provide further details as appropriate and answer the family's questions. Any queries should be answered as fully and accurately as possible.

Notifications—the supervising consultant must be contacted, if not already present. The patient's family doctor and the coroner should be informed by telephone at the earliest opportunity.

The anaesthetist—the rest of the operating list should be delayed until another anaesthetist and surgeon can take over.

Documentation—ensure that the medical record is complete and accurate. All entries in the patient's notes should be dated and signed. Details of the case should be clearly documented on an incident form (or equivalent) and copies delivered to the medical director and Clinical Director. A copy should also be retained by the anaesthetist for the medical defence organisation. These should not be filed in the case notes.

The mentor—a senior colleague should be allocated to act as mentor for the anaesthetist to provide guidance and support. The mentor should help with the notifications, assist in the compilation of reports, liaise with the anaesthetist's family, and offer support as necessary.

The theatre team—a debriefing session should be arranged to help the staff understand the event and come to terms with it. Group counselling may help to reduce post event psychological trauma.

Speak to a senior colleague for guidance and support. Consider asking a senior consultant or the Clinical Director to see the patient with you as the patient may value their advice and you may value their reassurance.

Apologise—saying sorry is not an admission of liability. Patients will appreciate your concern. However, do not apologise for the actions of others, or blame anyone without allowing them to comment.

Documentation—always make a detailed entry in the patient's notes of any dissatisfaction expressed and the action taken in response. Discuss with the Trust complaints manager.

The Trust will have an experienced manager who has responsibility for complaints who should be contacted.

Inform your medical defence organisation who will provide advice and support.

Record keeping—keep a full account of the details of the incident.

Leave a forwarding address if you move. A legal claim may be made many months after the event.

Grade and position held (including duration).

Full names and positions of others involved (patients, relatives, staff ).

Date(s) and time(s) of all the relevant matters.

Brief summary of the background details (e.g. patient's medical history).

Full and detailed description of the matters involved.

Date and time that your statement was made, and your signature on every page.

Copies of any supporting documents referred to in the statement (initialled by you).

Facts. Keep to the facts, particularly those that determined your decision-making, and avoid value judgments.

Avoid hearsay. Try to avoid including details that you have not witnessed yourself. If reference has to be made to such information, record the name and position of the person providing it to you, when it was provided, and how.

Be concise. State the essential details in a logical sequence and avoid generalisations.

Relevance. Include only the details required to understand the situation fully.

Avoid jargon. Give layman's explanations of any clinical terms used and avoid abbreviations.

Injuries may be the result of ballistic injuries from improvised explosive devices (IEDs), penetrating injuries from gun shot wounds, or other events such as road traffic accidents.

Military medical care starts immediately with soldiers trained to apply tourniquets, stop bleeding, and administer analgesia. More advanced first aid is given by the Combat Medical Technician (CMT). Uncontrolled haemorrhage is a common cause of death in conflict.

Early intervention in the battlefield area and moving the patient rapidly by air to an emergency medical facility is making a major impact on survival.

Simultaneous damage control resuscitation (DCR) and damage control surgery (DCS) followed by a short period of stabilisation in intensive care is the norm prior to onward transportation to Role 4 base hospital at Birmingham. This all occurs within 24hr of injury.

Anaesthetists are expected to work in a wide range of roles, including being deployed via land, sea, or air, parachute and helicopter insertion, life-threatening exposure to conflict in our Pre-Hospital Care role, and extremes of cold/heat.

Facilities for military anaesthesia are designed to be highly capable but mobile, allowing setting up of full trauma resuscitation/surgery facilities within 45min.

Anaesthesia includes intravenous, drawover, and regional/local anaesthesia techniques.

DCR relies on excellent, effective, and current communication between personnel: medical emergency response team, emergency department, anaesthesia, surgery, nursing, and laboratory teams. Ensure everyone in the resuscitation area or theatre is aware of their role, including a ‘blood runner’, rapid infusor operator, and blood product scribe. Be clear who is the resuscitation team leader.

Optimal preoxygenation.

Ketamine at a dose of 0.5–2mg/kg (racaemic) or thiopental 10–50% normal dose.

Rocuronium 1.2mg/kg or suxamethonium 1.5mg/kg.

8mm cuffed oral ETT for adults.

Introducer preprimed in ETT with 10ml syringe attached.

Size 4 Macintosh blade and/or Glidescope/Airtraq.

‘Shock Packs’ [4 units each of thawed FFP and packed RBCs (PRBC)] are made available for each severely injured patient.

Give 1:1 ratio of warmed FFP:PRBCs.

Ensure one platelet apheresis pool is made available and give early if anticipated blood product demand is high. Giving 1 platelet pool every 4–5 FFP:PRBCs equals a 1:1:1 optimum ratio.

Give 15mg/kg tranexamic acid ASAP and repeat every 10 transfused units until bleeding stops.

Give 10ml 10% calcuim chloride every 5 units or if ionised calcium <1.0mmol/l.

Aim for a systolic blood pressure of no more than 90mmHg until haemorrhage control is gained (clot preservation).

Avoid vasoconstrictors in the early period and administer blood products until a systolic blood pressure of 90mmHg is achieved.

Change from ‘Shock Packs’ to type-specific blood ASAP.

Further resuscitation should be guided by base deficit/lactate clearance and RoTEM thromboelastography (initial sample taken on admission). Repeating blood samples intelligently guides evolving resuscitation.

Use 50ml 50% glucose and 15IU insulin infusion to maintain potassium between 3.5 and 4.5mmol/l (especially important in blast injury and rapid restoration of blood loss).

Consider administering 1 pool of cryoprecipitate to maintain a fibrinogen level >1.0g/l (contains 10 donor units).

Use oesophageal temperature probe.

Fluid warming is the first priority.

Mattress heater.

Forced warm air blankets.

Head warmer.

Warm humidified breathing circuit.

For anaesthesia maintenance isoflurane at 0.4–0.6MAC with increasing boluses of fentanyl (2–3mg total dose for case) provides simple, cardiovasculary stable anaesthesia with a degree of vasodilatation to aid replacement of lost circulating fluid and lactate clearance.

If pH <7.1 consider tris-hydroxymethyl aminomethane (THAM) (dose in ml of 0.3M solution = base deficit × lean mass in kg) or sodium bicarbonate.

For resistant coagulopathy consider recombinant activated factor VII (rFVIIa) combined with 1 unit cryoprecipitate, 1 unit FFP, and 1 unit platelets administered simultaneously with 100µg/kg rFVIIa (‘Bastion Glue’) as recommended in the Surgeons General Policy on Massive Transfusion.

Additional platelets may be required in heavy platelet consumers—warn laboratory early.

Consider use of fresh whole blood for resistant coagulopathy.

Although patients initially may be hypocoagulable, they often become progressivley hypercoagulable. Venothromboprophylaxis should be instigated early when warranted.

Avoid crystalloids/colloids. If systolic BP <90mmHg give blood products.

Do not attempt arterial line insertion until systolic BP >90mmHg.

Resuscitation should not be delayed for tests or line insertion.

Constantly re-evaluate: when bleeding is controlled slow down the rate of blood and product infusion to avoid fluid-overloading the casualty—an important consideration in the presence of blast lung.

Emergency nurse

Two paramedics

<C> = control of life-threatening haemorrhage. Pneumatic/manual tourniquets. Pressure into wounds /haemostatic ribbon gauze.

A: Airway—rapid sequence induction if indicated.

B: Breathing— thoracostomy post RSI with IPPV/PEEP.

C: Circulation— large-bore IV/IO/central access. Used for PRBC/FFP administration. All fluids warmed with inline prehospital fluid warmers. Clam-shell thoracotomy if required (non-blast single penetrating chest trauma).

Hypothermia mitigation: this is achieved with the use of proprietary warming systems, e.g. ‘Blizzard Heat’.

Does not rely on electricity.

Low oxygen requirement—typically 1l/min during maintenance, reducing the need to transport oxygen cylinders.

Hypoxic gas mixture risk eliminated.

Simple to use.¹

OMV can use different volatile agents.

Use of end-tidal gas monitoring overcomes lack of temperature compensation.

Can be used for spontaneous or manual ventilation.

Suitable for patients >10kg.²

Not suitable for gaseous induction with sevoflurane.³

Inefficient.

Vaporisers can be knocked over and spill contents.

Drawover anaesthesia equipment may be combined with an oxygen concentrator allowing low-cost oxygen to be reliably produced (assuming electricity is available).

Conditions of anaesthesia in developing countries differ from military circumstances (well equipped and highly trained specialists treating severe trauma in well-run units).

Proposed location for administration of therapy (hospital, GP/clinic, home).

Risk of contamination of catheter.

Patient's clinical status (coagulation status, sepsis, CVS stability).

Risk of sclerosant drugs.

Long-term antibiotics.

Home TPN.

Haemodialysis.

Repeated blood transfusions or repeated venesection.

Midlines (10–20cm soft catheter) are inserted via the antecubital fossa, with the tip of the device situated in the upper third of the basilic or cephalic vein and short of the great vessels.

Non-cuffed, non-tunnelled central venous catheters (CVC) are used for resuscitation/central venous monitoring. Non-tunnelled CVCs are rarely used for >10–14d, due to the risk of sepsis. Antimicrobial-coated catheters are available. Use a single lumen catheter when possible.

Tunnelled non-cuffed catheters are used less frequently, as similar cuffed devices offer a more secure fixation and a potential antimicrobial barrier.

Tunnelled, cuffed, central venous catheters (‘Hickman type lines’) are tunnelled from the insertion site on either the chest or abdominal wall. They can be open ended or contain a two-way valve (‘Groshong catheter’). These are used for prolonged therapies and have a Dacron cuff which allows fibrotic tissue ingrowth to provide anchorage and a possible barrier to infection. It takes 3–4wk for fibrous adhesions to develop and hence should not be inserted for shorter use. Similar devices exist for dialysis (e.g. Tesio).

Subcutaneous (SC) ports made from either titanium or plastic offer a single or double injection port attached to a central catheter. A SC pocket is formed on the chest or abdominal wall to house the port. They are surgically placed and used for prolonged periods of intermittent therapy, e.g. antibiotics for cystic fibrosis. Popular for children. Enable bathing and immersion.

Choose site dependent on patient factors, previous access, and clinician experience.

Look for evidence of thrombosis or stenosis, previous scars from long-term access, and venous collaterals (suggest great vein stenosis). If doubt exists concerning vessel patency use ultrasound to assess access site. Formal venography is helpful in difficult cases.

Choose puncture sites and tunnel tract to avoid tight bends; if necessary use multiple puncture sites to avoid >90° bends and catheter kinks.

Particularly recommended for internal jugular but useful for all sites and ages.

Useful in context of difficult/repeated long-term venous access.

For subclavian access move lateral to junction of axillary/subclavian vein to allow visualisation with ultrasound.

Note patent vein at access site does not guarantee central vein patency.

Respiratory variation in vein size suggests patent central vein.

Measure catheter length required with correctly positioned guidewire (using fluoroscopy). Or lay on chest wall with tip over right side of sternal angle.

Take care with rigid sheaths and dilators to avoid central vessel damage. Do not insert too deeply (generally longer than required).

Pinch sheath on removal of obturator to avoid bleeding and air embolism (some are valved).

Sheaths readily kink—draw back until catheter passes.

Pass long, thin guidewire (70cm+, Terumo-coated type) through soft catheters to increase torque if difficulties passing centrally.

Screen guidewire, obturator sheath, and catheter insertion if any difficulty encountered. Use venography through needle, sheath, or catheter if uncertain as to position. 10ml diluted contrast (check allergy), e.g. Ultravist 120^®.

For fixed-length catheters (e.g. Groshong, dialysis) take care to choose correct length for site of access and adequate length of tunnel tract to ensure correct tip position in SVC.

Move catheter and cuff along tunnel tract to adjust catheter tip position.

Flush with saline/heparinised saline before and after use.

Image tunnelled section of line to look for kinks.

Minimise incision and pocket size by placing port anchor sutures within the pocket first and then slide port in over them and tie off (same principle as cardiac valve replacement).

Access is gained by a specific ‘non-coring’ needle and advancement through the silicone membrane to the reservoir below. Initial access to a port causes discomfort and EMLA® cream can be applied 30min before. There is a distinct clunk as the needle hits the back wall of the port after penetrating the membrane.

Leave access needle in situ if access required soon after insertion to avoid painful wound site (settles after a few days).

It is generally recommended that the tip should lie above the pericardial reflection (to avoid perforation and tamponade). The carina (or right main bronchus) can be used as a radiological landmark to define the approximate upper border of the pericardium.

It may not be possible to get an adequate catheter tip position above the carina in catheters from the left side (left internal jugular or subclavian) or the right subclavian due to the angulation of the distal catheter segment. Aim to have the last 3–6cm of catheter tip in the long axis of the SVC (this will approximate to the junction of SVC/RA or upper RA in such cases).

ECG guidance may be used to confirm central position but does not ensure good tip position in SVC (may be angled against vein wall), particularly with left-sided catheters.

Catheter tip may move between lying and sitting/standing. Assess on inspiration and expiration with the patient table flat. It will generally appear much further centrally on supine/head down imaging than on an erect PA film with deep inspiration.

When used in patients at high risk of thromboembolism, therapeutic doses of warfarin or low molecular weight heparin (LMWH) may reduce the frequency of catheter-related thrombosis.

Beware: some units still lock catheters with strong heparin (e.g. dialysis catheters)—always aspirate catheter and discard before use.

Thrombosed catheters can be unblocked with urokinase (5000U). Suction all air through three-way tap to collapse catheter and create vacuum. Then inject urokinase diluted in 2ml saline, and repeat sequence to get fluid into catheter. Avoid excess pressure that can rupture catheter.

Heavily infected catheters usually pull out as the infection breaks down adhesions.

Push and pull catheter to palpate and visualise cuff shape and tethering. It is difficult to feel cuff if it is just inside the exit site.

Inject generous LA around cuff site and tunnel tract.

Cut down (1–2cm incision sufficient) just to the vein side of the cuff. Use forceps to feel catheter as solid structure that rolls under the forceps (incision too small for finger). Free up and remove venous section first; a thin fibrin sheath/capsule will need to be incised to free the catheter. Pull catheter out of vein.

Then dissect around cuff to free adhesions.

Try to avoid sharp dissection until the venous section of catheter is removed to reduce risk of embolisation from cut catheter (catheters can pass to RV/PA).

Similar considerations apply to port removals where the port and catheter are encased in a tough fibrous sheath.

Catheter blockage. Catheters can rupture between clavicle and first rib (pinch off) or become thrombosed (see above).

Fibrin sleeve formation commonly obstructs aspiration of blood but still allows injection of fluids.

Venous thrombosis usually requires catheter removal and anticoagulation.

Vein stenosis and venous collateral formation are often asymptomatic due to gradual obstruction. Can be reopened by radiological stenting.

Valved catheters (Groschong) or those with fibrin sleeve covering the tip may not give CVP waveform and may cause intermittent drug bolusing during infusion (avoid for vasoactive drugs).

Ports and other catheters are good options for a child requiring repeated IV anaesthetic induction.

The probe is inserted into the oesophagus via the nose (preferable) or mouth.

When the tip of the probe is lying 35–40cm from the teeth a characteristic Doppler signal can be located by rotating the probe and moving it up or down the oesophagus.

When the probe is correctly focused the signal should be a well-defined triangle with a black centre surrounded by red and then some white in the trailing edge of the waveform (see figure 37.5).

Stroke volume (SV). Change in SV following a fluid challenge provides the best indicator of fluid responsiveness in an anaesthetised patient. A 10% increase after a 3ml/kg fluid challenge implies responsiveness and should prompt a further fluid challenge.

Corrected flow time (FTc). The duration of forward blood flow during systole is measured as the flow time and is dependent on the heart rate. To mitigate this the flow time is divided by the square root of the heart rate to produce the corrected flow time (FTc) which then becomes a useful marker of preload and afterload. A low FTc implies that the filling or emptying of the left ventricle is impaired and this is most commonly seen with hypovolaemia, although obstruction from mitral stenosis or pulmonary embolism will give similar results.

Turn the volume up to focus the probe initially. The sharpest sound with the best pitch is invariably the optimum waveform.

Adjust the following:

Always visually check that each waveform is being counted, i.e. it has a small white triangle in each corner.

Patients having general anaesthesia and/or epidural may have an FTc approaching 400ms if dilated and well filled.

It is a dynamic monitor and as such must be refocused prior to each reading.

Sudden reduction in FTc can occur under anaesthesia due to factors other than fluid balance. Surgical compression of the aorta (packs/retractors) and alteration in muscle tone (insufficient muscle relaxant) can cause a sudden change that should not mandate a fluid challenge.

Low FTc: this most commonly represents hypovolaemia and the circulation should be challenged to achieve an FTc of 330–360ms. This is not always possible to achieve, especially in beta-blocked patients, and caution needs to be employed to avoid excessive fluid administration. For this reason the manufacturers recommend that fluid therapy in theatre be guided predominantly by SV changes.

Low PV: consider use of a positive inotrope.

Low PV and low FTc: consider agents/manoeuvres to decrease afterload, e.g. GTN, peripheral warming, or reduction of vasoconstrictors.

High-risk patients

Haemodynamic instability

Severe aortic coarctation.

Surgery requiring aortic cross-clamp.

Known pharyngo-oesophageal pathology.

Severe bleeding diatheses.

Patient State Index. Developed by computer analysis of large numbers of EEGs throughout the anaesthetic process to establish the electrophysiological variability of anaesthetic depth related EEG changes. Calculates an index of hypnosis from patient's EEG.

Depth of anaesthesia (DoA) monitors are credible adjuncts to patient care. Their uptake is primarily constrained by cost. Current research questions include the impact of DoA monitoring on patient outcome and the unresolved issue of whether they are any more effective in preventing awareness than standard anaesthetic techniques when effectively applied, especially with highly protocolised care.

A computer-controlled ramped increase in workload.

A calibrated pneumotachograph to measure gas flow and composition.

Continuous 12-lead ECG recording.

Someone trained to conduct and interpret the test.

Informed decision making.

Perioperative management, including ICU/HDU requirement.

Diagnosis and quantification of respiratory and cardiac disease.

Risk reduction by guiding interventions before, during, and after surgery.

Has the most rapid onset of action of all relaxants.

Used when fast onset and brief duration of paralysis are required.

A dose of 1–1.5mg/kg is recommended.

Metabolised by plasma cholinesterase (see below).

Raised intraocular pressure: this is of no clinical significance in most patients but may be important in poorly controlled glaucoma or penetrating eye injuries ( p. 698).

Hyperkalaemia: serum potassium increases by 0.5mmol/l in normal individuals. This may be significant with pre-existing elevated serum potassium. Patients with burns or certain neurological conditions, e.g. paraplegia, muscular dystrophy, and dystrophia myotonica, may develop severe hyperkalaemia following administration. Patients who have sustained significant burns or spinal cord injuries can be given suxamethonium, if necessary, within the first 48hr following injury. Thereafter there is an increasing risk of life-threatening hyperkalaemia, which reduces over the ensuing months. Avoid suxamethonium until 12 months have elapsed following a burns injury. There may be a permanent risk of hyperkalaemia with upper motor neuron lesions.

Bradycardias, particularly in children, or if repeated doses of the drug are given. Can be prevented or treated with antimuscarinic agents, e.g. atropine and glycopyrronium.

Malignant hyperthermia (see pp. 270–275): suxamethonium is a potent trigger for this condition in predisposed individuals.

High or repeated doses (probably >8mg/kg) may create dual block which will prolong paralysis.

Plasma cholinesterase (pseudocholinesterase or butyrylcholinesterase): capable of hydrolysing a variety of esters. A physiological function for this enzyme has yet to be discovered, but many drugs either interfere with its action or are metabolised by it. Plasma cholinesterase is synthesised in the liver, has a half-life of 5–12d, and metabolises 70% of a 100mg bolus of suxamethonium within 1min. Genetically, it is encoded on the long arm of chromosome 3. Several variant genes can occur which result in reduced enzyme activity:

Administration of drugs that share the same metabolic pathway, and therefore compete with suxamethonium for the enzyme, e.g. esmolol, monoamine oxidase inhibitors, methotrexate.

Presence of anticholinesterases (e.g. edrophonium, neostigmine, ecothiopate eye drops), which inhibit plasma cholinesterase as well as acetylcholinesterase.

Pregnancy, where the enzyme activity is reduced by 25%.

Plasmapheresis and cardiopulmonary bypass.

Cocaine: toxicity is more likely.

Plasma cholinesterase also partially metabolises diamorphine, esmolol, and remifentanil. Low enzyme activity does not currently appear to complicate their use.

Medium-acting compounds which are effective for ∼40min (atracurium, vecuronium, rocuronium, cisatracurium).

Long-acting compounds which have a clinical effect for 60min (pancuronium, d-tubocurarine).

Many of the benzylisoquinoliniums release histamine, the amount of histamine released being related to the speed of injection. Avoid these drugs in severely atopic or asthmatic individuals. Cisatracurium, however, does not cause histamine release.

Like suxamethonium, mivacurium is metabolised by plasma cholinesterase. Patients with reduced levels of this enzyme will exhibit prolonged paralysis.

Cisatracurium and atracurium are mainly broken down by Hoffman degradation, a process that is pH and temperature dependent. This metabolism is not affected by the presence of renal failure, so these relaxants are ideal in those with renal impairment.

Rocuronium, at doses of 0.6mg/kg or greater, gives satisfactory intubating conditions within 60s. Its speed of onset is significantly faster than all other non-depolarising relaxants.

Mivacurium is useful for short procedures. It does not need to be reversed routinely, providing sufficient time has elapsed (>20min) after a bolus and neuromuscular monitoring is used.

Monitor relaxants routinely. This will help you decide when to top-up, when to reverse, and when muscle function has returned.

Maintenance doses of NDMRs should be approximately a fifth to a quarter of the initial dose.

Anticipate relaxant drugs wearing off, rather than waiting for patient to cough or move.

Do not attempt to reverse intermediate-duration NDMRs within 15min of administration.

Do not wait for suxamethonium to wear off before giving an NDMR. On the very rare occasion that a patient has reduced cholinesterase levels, administering an NDMR will make little difference to the outcome.

Common peroneal nerve. Stimulated immediately below the head of the fibula. Foot dorsiflexion is assessed.

Facial nerve. Stimulated with electrodes placed in front of the hairline on the temple.

Double-burst stimulation (DBS) is a stronger stimulus, where two short bursts of 50Hz tetanus are separated by 750ms. DBS and TOF ratios correlate well, but fade is more accurately assessed with DBS, and an absence of fade is usually good evidence of reversal.

Post-tetanic count can be used to assess deep relaxation when the TOF is zero. A 50Hz tetanic stimulation is applied for 5s followed by 1Hz single twitches. Reversal should be possible at a post-tetanic count of 10 or greater.

Nerve stimulator: an acceptable recovery from block occurs when the TOFR has reached 0.9 or greater. The absence of any detectable fade with double-burst stimulation indicates that the patient has reasonable recovery.

At the completion of surgery, normal neuromuscular transmission can be facilitated by the use of anticholinesterase drugs.

Reversal agents should not be given until there is evidence of return of neuromuscular transmission, e.g. at least 2 TOF twitches, 1 DBS twitch, or a post-tetanic count greater than 10. Clinically, this might include evidence of breathing or spontaneous muscle movement. Intense neuromuscular block may not be reversible.

Patients who are inadequately reversed exhibit jerky and uncoordinated muscle movements. If awake, they may appear dyspnoeic and anxious. If residual block is confirmed by TOF or DBS, one further dose of reversal agent may be administered. Agitated patients with reasonable respiratory function and otherwise normal vital signs may be given a small dose of a sedative (e.g. midazolam 1–5mg) whilst awaiting the return of full muscle function. If the block persists, or if the patient is very distressed, anaesthesia, intubation, and artificial ventilation should be undertaken and the cause sought.

Anticholinesterase drugs act at both nicotinic and muscarinic sites, thus producing unwanted side effects which include salivation, bradycardia, bronchospasm, and increased gut motility. They are therefore usually administered with antimuscarinic agents (atropine 10–20µg/kg, glycopyrronium 10–15µg/kg).

A novel reversal drug (sugammadex) has been released which rapidly immobilises and inactivates certain aminosteroid NDMRs, particularly rocuronium (and vecuronium). Larger doses (4mg/kg) can reverse deep rocuronium blockade, where there is no response to TOF or DBS. In doses of 16mg/kg, immediate reversal of an intubating bolus of rocuronium is possible. Conventional reversal drugs cannot do this. Its use is currently limited by expense.

In 1996 Thrombelastograph and TEG became registered trademarks of Haemoscope Corporation and these terms are now used to describe the assay performed on their machine. Pentapharm makes another machine using slightly different technology and uses the terms thromboelastometry and ROTEM.

The TEG uses whole blood and kaolin to activate the test. Once the sample is taken from the patient it must be tested within about 5min.

The ROTEM uses a citrated sample and a number of different activating reagents (INTEM, EXTEM, HEPTEM, FIBTEM, and APTEM). Once the sample is taken from the patient and placed in a citrated bottle it must be tested within 4hr.

Routine coagulation tests are performed in the laboratory and therefore may take up to 45min to be completed and reported. TEG machines are usually placed in a clinical location, allowing the evolving trace to be viewed and consequentially results obtained rapidly.