Sedation

A state of CNS depression during which verbal contact with the patient is maintained. Achieved with Entonox, oral/i.v. benzodiazepines, i.v. methohexitone.

Cardiovascular side-effects

Dysrhythmias. These are common due to sympathetic and parasympathetic activity, high levels of endogenous catecholamines, halothane and airway obstruction with hypoxia and hypercarbia:

They mostly occur during surgery and are worse during trigeminal nerve stimulation. Atropine increases the incidence of dysrrhythmias.

Less common with i.v. induction than with gaseous induction. Less common with volatile agents other than halothane.

More common following recent Coxsackie B infection due to (?) viral myocarditis.

Arrhythmias may be the primary cause of high mortality seen with dental GAs.

Fainting. Only in conscious patients! May need large doses of atropine. Abandon procedure because CVS instability persists for up to 90 min.

High mortality in erect patients was attributed to unrecognized fainting, but mortality is the same in supine patients. Supine position is associated with more pharyngeal soiling. It is now recommended that all surgery should be performed in the supine position which gives better CVS stability.

Myringotomy

This is a short, relatively painless operation. Premedication is not usually necessary.

Chronic otitis media is often associated with upper respiratory tract infection. Morbidity not increased with uncomplicated URTI if mask rather than intubation used. Need postoperative O₂ if oxygen saturation <93% on room air.

Middle ear surgery

Careful positioning is required to avoid obstruction of venous drainage of the head. Tympanoplasty and mastoidectomy usually require identification of facial nerve. Therefore, avoid long-acting neuromuscular blocking drugs.

Use hypotensive anaesthesia to minimize bleeding. Maximum recommended safe dose of adrenaline = 0.1 mg/10 min.

Avoid N₂O which diffuses into the middle ear to cause expansion, or on cessation diffuses out of the middle ear to cause negative pressure and disruption of ossicles.

Consider prophylactic antiemetics.

Anaesthesia of the nasal cavities

Tonsillectomy

Avoid premedication if tonsils are large or there is a history of sleep apnoea. Use gas or i.v. induction. Either deep gaseous intubation (patient more drowsy postoperatively) or suxamethonium. Use throat pack and endotracheal tube. Spontaneous respiration tends to hypoventilation with risk of arrhythmias, especially with halothane.

Extubate awake (protective reflexes), with head-down in left lateral position.

Postoperative haemorrhage. Affects 0.5%; 75% of postoperative haemorrhages occur within 6 h of surgery. Main problems are:

Assessing the patient can be difficult. Tachycardia due to hypovolaemia may also be due to anxiety or pain. Blood loss is usually underestimated, as most is swallowed. Establish i.v. access, check BP sitting and lying (postural hypotension with hypovolaemia), check haematocrit and cross-match blood.

There are two approaches to induction:

Both approaches need a selection of laryngoscope blades, stylettes, range of ETTs, two suction units (one may become blocked with clot), emergency tracheostomy kit and tipping trolley.

Pass NG tube and aspirate stomach prior to extubation.

Adenoidectomy

Usually performed in conjunction with tonsillectomy. Not as painful. May cause nasopharyngeal obstruction and obligate mouth breathing.

Obstructive sleep apnoea

Grossly hypertrophied tonsils can cause partial upper airway obstruction when awake and complete obstruction during sleep. Associated with obesity, micrognathia (e.g. Pierre–Robin syndrome) and neuromuscular disorders (e.g. cerebral palsy). May present as failure to thrive, snoring, daytime somnolence, developmental delay, recurrent chest infections and, if severe, cor pulmonale. Airway obstruction may persist post-tonsillectomy.

Peritonsillar abscess (quinsy)

The infected tonsil forms an abscess in the lateral pharyngeal wall with associated trismus and difficulty in swallowing. The abscess does not usually interfere with the airway, but there is a risk of rupture and aspiration of contents. Drainage under LA, otherwise treat as for epiglottitis. Consider tracheostomy under LA if abscess is likely to rupture on intubation.

Preoperative

Assess cardiovascular and renal status. Optimize respiratory function with antibiotics, bronchodilators, physiotherapy and consider drainage of ascites. Correct coagulation with FFP, cryoprecipitate, vitamin K and platelets.

Premedication

Avoid if possible.

Monitoring

Routine monitoring, arterial line, CVP, urinary catheter, nerve stimulator, ± PCWP.

Induction

Use small amounts of thiopentone or midazolam.

Maintenance

Use isoflurane/sevoflurane/desflurane in oxygen. High F_io₂ needed because of pulmonary shunting. Avoid hyperventilation which increases mean intrathoracic pressure, thus reducing hepatic blood flow, accelerates formation of ammonia, causing hepatic encephalopathy, and increases urinary potassium loss through respiratory alkalosis. Hepatic blood flow is proportional to mean arterial pressure. Keep CVP <5 mmHg to reduce haemorrhage secondary to venous congestion.

Neuromuscular blockade with atracurium or pancuronium. Reversal with normal doses of anticholinesterases. Avoid rocuronium which has prolonged action.

Maintain high urine output to protect against renal failure. Avoid excess sodium load in i.v. fluids to prevent dilutional hyponatraemia.

Hepatic disease reduces synthesis of coagulation factors and inhibitors, and causes quantitative and qualitative platelet defects and hyperfibrinolysis. Massive haemorrhage a particular risk with cirrhosis, steatosis, and after chemotherapy. Exacerbated by acidosis, hypothermia and hypocalcaemia. Use of cell salvage in malignancy is controversial. Anti-fibrinolytics (e.g. tranexamic acid) reduces perioperative blood loss.

Postoperative

IPPV may be necessary until patient is rewarmed and stabilized. Remove lines as soon as possible to reduce risk of infection. Analgesia with small doses of opioids. Remifentanil avoids accumulation of active opioid metabolites. Regional block may reduce requirements, provided clotting is normal.

Watch for hypoglycaemia as a result of impaired hepatic mobilization of glucose. Secondary hyperaldosteronism is common (sodium and water retention and oedema), which is minimized by restriction of sodium intake and treated with diuretics.

Aqueous humour

Made by ciliary plexus and secreted into anterior chamber. Absorbed through the trabecular meshwork into the canal of Schlem.

Intraocular pressure (IOP)

Normal value 15–25 mmHg. Once the eye is opened, IOP is equal to atmospheric pressure. Hypoxia, hypercapnia, coughing and vomiting all increase IOP.

Oculocardiac reflex

Reflex pathway runs from the long and short ciliary nerves via the ciliary ganglion to the ophthalmic division of the trigeminal nerve (V) and then to the Gasserian ganglion. From here, the pathway runs to the trigeminal sensory nucleus in the brainstem, to the motor nucleus of the vagus (X) in the medulla, through the reticular formation and finally to the heart via the vagus nerve.

Causes bradycardia, asystole, PVCs, A–V block, VT and VF. It is more marked and frequent in children, particularly during squint surgery.

Reflex fatigues quickly with cessation of stimulus.

Prophylaxis with glycopyrrolate is as effective as atropine.

Requirements

Advantages of regional block over GA

Premedication

Monitoring

Often in a dark room (to prevent glare interfering with surgical microscope) with minimal access to patient. Expose limb and illuminate a limb to allow access to a pulse and observe for cyanosis.

Induction

Propofol decreases IOP more than thiopentone and causes less nausea and vomiting. Laryngeal mask airway (LMA) results in less rise in IOP compared with ETT and less postoperative coughing and sore throat. If patient is ventilated, ETT avoids risks of regurgitation, but spray cord with local anaesthetic to reduce coughing. Tape ETT in place because a tie causes venous obstruction to drainage of head, raising IOP.

Smooth extubation to avoid coughing by extubating deep, deflating cuff before reversal and using lidocaine 1.5 mg/kg pre-extubation.

Ecothiopate (organophosphate – no longer available) inhibited plasma cholinesterase and prolonged action of suxamethonium. Avoid suxamethonium with myotonic dystrophy.

Keep IOP low by:

Nitrous oxide. Intraocular bubbles of sulphur hexafluoride (SF₆) or perfluoropropane (C₃F₈) are used in surgery for detached retina to push the retina against the choroid. Nitrous oxide will cause rapid expansion of the bubble if used within 10 days.

Local anaesthetic solution

Use:

Less painful injection if solution warmed to 35°C.

Retrobulbar and peribulbar blocks are equated with spinal and epidural blocks, respectively.

Retrobulbar block. First described by Atkinson in 1955. Patient looks straight ahead. Use a 25G 40 mm blunt needle.

The popularity of retrobulbar block has declined due to a greater risk of neurovascular damage compared with peribulbar block.

Peribulbar block. First described by Davis and Mandel in 1986. Aim to keep the needle always at a tangent to the globe, advancing the tip no further than the equator of the globe, outside the muscle cone. Uses larger dose of LA and has a longer onset time. Use a 25G 25 mm blunt needle.

Compress eyeball for 10 min after injection to aid spread of LA using small pneumatic/lead balloon strapped over eye.

Block of facial nerve is not usually required.

Sub-Tenon’s (episcleral) block Least painful of all blocks (99.1% patients report a painless injection). Topical LA to conjunctiva. Ask patient to look up and out. Using forceps, take a deep bite of conjunctiva and Tenon’s capsule in the inferonasal quadrant, 5–7 mm from the limbus. Make a 2 mm opening halfway between the forceps and the globe, with scissors. A blunt, curved 19G, 25 mm sub-Tenon’s cannula is passed into the tunnel and advanced slowly keeping the tip hugging the sclera until the syringe is vertical to a depth of 15–20 mm in the inferonasal quadrant. This delivers anaesthetic posterior to the equator of the globe. Globe akinesia not always obtained because of smaller volumes of LA. Chemosis and subconjunctival haemorrhage more common.

Complications of regional blocks

Of 60 000 annual LA operations, life-threatening complications occur in 1:750. There are fewer complications with peribulbar block, but less akinesia.

• Penetration of the eye, causing:

– intraocular haemorrhage

– immediate/delayed retinal detachment

– intraocular toxicity of local anaesthetic drugs and the following symptoms:

movement of the eye with the needle

acute pain

sudden loss of vision

loss of ocular tone.

Preoperative

Most elderly patients have co-existing diseases. Carry out cardiovascular and respiratory assessment. Treat other pathology as necessary, e.g. dehydration, diabetes, renal failure, infection. Osteoarthritis and joint immobility are common. Outcome is improved if surgery takes place between 24 and 36 h after admission. Excessive delays risk pressure sores, DVT and pulmonary embolus (PE), pneumonia and an overall increase in mortality. Therefore, do not prolong patient optimization longer than necessary.

Anaesthetic technique

Over the past decade, several studies have shown that regional anaesthesia is associated with reduced morbidity and mortality. Mechanisms may include:

Preoperative autologous blood donation, cell salvaging and mild deliberate hypotension reduce transfusion requirements. Mild hypothermia (35.0 versus 36.6°C) has been shown to increase blood loss during hip arthroplasty.

Bone cement

Hypotension and cardiac arrest were initially attributed to free methylmethacrylate monomer forced into circulation during insertion of cement. However, they are now thought to be due to fat, air, platelet and marrow embolization with V/ mismatching and release of vasoactive substances from the lungs. Severe pain during intramedullary nailing may also contribute.

Hypotension during cement insertion is more common with increasing age, uraemia and pre-existing hypertension. Incidence is reduced if normovolaemia is maintained during cement insertion.

Fat embolism syndrome (FES)

Fat is released into the circulation in most patients from long bones at the time of fracture or during intramedullary nailing to cause asymptomatic embolization. However, in 2% of patients following femoral fractures, 0.1% after hip/knee replacements, and as many as 90% of multiple trauma patients, the degree of embolization may be sufficient to cause a triad of symptoms (which are not always present):

Severe FES may cause cardiovascular collapse, multiorgan failure and death. Pathophysiological changes occur in three steps (Fig. 4.1). FES also reported with burns, acute pancreatitis, hepatic failure, bone marrow harvest and extra-corporeal circulation.

Figure 4.1 Pathophysiological changes in severe fat embolism syndrome.

Prophylaxis. Surgical measures to minimize intramedullary pressure. Ensure adequate hydration. Consider delaying medullary reaming in major trauma patients.

Treatment is non-specific and supportive. Early recognition is vital (desaturation, petechiae, confusion, hypotension). Consider bronchoalveolar lavage for diagnostic cytology. Oxygen, fluid management, anticoagulation. Steroids are unproven. Aspirin may improve blood gases, coagulation protein levels, and platelet count. Heparin is known to clear lipaemic serum by stimulating lipase activity and has been advocated for the treatment of FES, although may risk bleeding in trauma patients.

Postoperative hyponatraemia

Iatrogenic hyponatraemia is particularly common following orthopaedic surgery due to fluid overload from 5% dextrose, which after metabolism of dextrose leaves free water. Compounded by:

Some 20% of patients with symptomatic hyponatraemia die or suffer serious brain damage. Brain damage has been reported with sodium as high as 128 mmol/L. Postmenopausal women are usually not symptomatic until sodium <120 mmol/L.

Early symptoms. Weakness, nausea, vomiting and headache.

Late symptoms. Encephalopathy, convulsions, respiratory arrest, brain damage. Aim to raise serum sodium 1–2 mmol/L per hour until symptoms resolve. Risk of treatment is far less than risk of osmotic demyelination from treatment. Consider fluid restriction or hypertonic saline. Loop diuretics (e.g. furosemide) enhance free water excretion.

DVT prophylaxis

Without DVT prophylaxis, 50–80% of elderly patients will develop a DVT, and 1–5% die from pulmonary embolism. Compression stocking, aspirin and early mobilization all reduce DVT risk further.

Nice Clinical Guideline 92

Venous Thromboembolism: Reducing the Risk of Venous Thromboembolism (Deep Vein Thrombosis and Pulmonary Embolism) in Patients Admitted to Hospital, January 2010

Assessing the risks of VTE and bleeding

1. Assess all patients to identify those who are at increased risk of venous thromboembolism (VTE)

Patients who are at risk of VTE

Medical patients

• If mobility significantly reduced for ≥3 days or

• If expected to have ongoing reduced mobility relative to normal state plus any VTE risk factor.

Surgical patients and patients with trauma

• If total anaesthetic + surgical time >90 min or

• If surgery involves pelvis or lower limb and total anaesthetic + surgical time >60 min or

• If acute surgical admission with inflammatory or intra-abdominal condition or

• If expected to have significant reduction in mobility or

• If any VTE risk factor present.

VTE risk factors (for women who are pregnant or have given birth within the previous 6 weeks, see full guidance for more detail)

• Active cancer or cancer treatment

• Age >60 years

• Critical care admission

• Dehydration

• Known thrombophilias

• Obesity (BMI >30 kg/m²)

• One or more significant medical comorbidities (for example: heart disease; metabolic, endocrine or respiratory pathologies; acute infectious diseases; inflammatory conditions)

• Personal history or first-degree relative with a history of VTE

• Use of HRT

• Use of oestrogen-containing contraceptive therapy

• Varicose veins with phlebitis

2. Assess all patients for risk of bleeding before offering pharmacological VTE prophylaxis

Patients who are at risk of bleeding

All patients who have any of the following

• Active bleeding

• Acquired bleeding disorders (such as acute liver failure)

• Concurrent use of anticoagulants known to increase the risk of bleeding (such as warfarin with INR >2)

• Lumbar puncture/epidural/spinal anaesthesia within the previous 4 h or expected within the next 12 h

• Acute stroke

• Thrombocytopenia (platelets <75 × 10⁹/L)

• Uncontrolled systolic hypertension (≥230/120 mmHg)

• Untreated inherited bleeding disorders (such as haemophilia or von Willebrand’s disease)

3. Assess all patients for risk of bleeding before offering pharmacological VTE prophylaxis. Do not offer pharmacological VTE prophylaxis to patients with any of the risk factors for bleeding

4. Reassess risks of VTE and bleeding whenever the clinical situation changes.

Reducing the risk of VTE

• Encourage patients to mobilise as soon as possible.

• Offer one of the following to those at increased risk of VTE:

– Fondaparinux sodium

– Low molecular weight heparin

– Unfractionated heparin for patients with renal failure.

Patient information and planning for discharge

• On admission, offer patients verbal and written information on VTE.

• As part of the discharge plan offer patient information on the symptoms and signs of VTE and the need for appropriate post-dicharge therapy.

Mechanical prophylaxis

• On admission to hospital, offer surgical inpatients mechanical VTE prophylaxis (see full guidance for more detail).

– Anti-embolism stockings. Use thigh-length graduated compression/anti-embolism stockings, unless contraindicated (e.g. diabetic neuropathy, peripheral vascular disease, peripheral vascular disease).

– Foot impulse and intermittent pneumatic devices. Intermittent pneumatic compression devices may be used as an alternative. These devices should be used for as much time as is possible.

Pharmacological prophylaxis

• Consider offering additional mechanical or pharmacological VTE prophylaxis if patient is at risk of VTE (Figs 4.2,4.3).

Figure 4.2 Non-orthopaedic surgery.

Figure 4.3 Orthopaedic surgery.

Other anaesthetic-related issues

• Advise patients to consider stopping combined oral contraceptives 4 weeks before elective surgery.

• Carefully plan the timing of pharmacological prophylaxis if using regional anaesthesia to minimize the risk of haematoma.

Other strategies

• Do not allow patients to become dehydrated during their stay in hospital.

• Consider using regional anaesthesia if appropriate as it reduces the risk of VTE compared with GA.

Pharmacokinetic and pharmacodynamic changes

These changes result in hypertension, water retention, peripheral oedema and hyperdynamic circulation; also accumulation of ionized, water-soluble compounds, e.g. non-depolarizing neuromuscular blockers, digoxin, atropine, neostigmine, water-soluble β-blockers, e.g. atenolol.

Common conditions associated with chronic renal failure

CVS. Hypertension, LVF exacerbated by A–V fistula, accelerated atherosclerosis causing ischaemic heart disease and peripheral vascular disease. Pericardial effusion and cardiomyopathy secondary to uraemia and dialysis.

Respiratory. Peritoneal dialysis causes diaphragmatic splinting, atelectasis and shunting. Respiratory infection is common. Fluid overload between periods of dialysis, causing pulmonary congestion.

GI. Delayed gastric emptying and increased gastric acid secretion. High risk of aspiration. GI bleeding. Deranged liver function secondary to transfusion-related hepatitis.

Neurological. Peripheral and autonomic neuropathy. Mild uraemic encephalopathy.

Haematology. Normochromic normocytic anaemia due to decreased erythropoietin, bone marrow depression from anaemia, iron, folate and B₁₂ deficiency and increased red cell fragility. Decreased O₂ delivery compensated for by ↑ CO, metabolic acidosis and ↑ 2,3-DPG, shifting O₂ dissociation curve to the right. Defective platelet function, increased factor VIII and fibrinogen, and decreased antithrombin III result in hypercoagulable state despite increased bleeding time.

Post-dialysis. Residual heparinization for 10 h post-dialysis. Large fluid shifts may cause hypotension, nausea and vomiting.

Other. Metabolic acidosis, hyperkalaemia, hypomagnesaemia, hypocalcaemia, hyperphosphataemia, bone decalcification and carbohydrate intolerance.

Specific drugs

Preoperative

Measure baseline creatinine clearance. Preoperative haemodialysis to correct fluid and electrolytes, avoid cannulae in limbs (in case they are needed for fistula formation), correct hypertension and dehydration, control diabetes, administer anti-aspiration premedication.

Monitoring

ECG, invasive BP, pulse oximetry, CVP, urinary catheter, ± PCWP. Regular blood glucose.

Induction

Thiopentone, etomidate or propofol is suitable. Suxamethonium may increase K⁺ 0.5 mmol.L⁻¹. Intravenous opioids (fentanyl/alfentanil/remifentanil) useful to blunt stress response to intubation in hypertensive patients.

Maintenance

Patients with CRF are acidotic, so avoid spontaneous respiration. F⁻ produced by metabolism of methoxyflurane was nephrotoxic. F⁻ levels with enflurane reached 75% of nephrotoxic threshold. Much less F⁻ produced by sevoflurane >isoflurane, with levels below nephrotoxic threshold. Desflurane does not increase F⁻ levels. N₂O is safe. Effective antihypertensive drugs are GTN or trimetaphan. Sodium nitroprusside in end-stage renal failure (ESRF) may cause cyanide toxicity.

Use neuromuscular blockers whose excretion is independent of renal function (e.g. atracurium, vecuronium, rocuronium). Pancuronium and morphine prolonged as mostly renal excretion.

Keep well hydrated. Replace fluid loss with salt-containing solutions (avoid Hartmann’s as this contains K⁺). Low threshold for blood transfusion since patient is already anaemic.

Regional anaesthesia

Spinal and epidural anaesthesia can maintain renal blood flow if hypotension is avoided. Bladder innervation via SNS from T₁₂–L₃ and PNS from S₂–S₄. Therefore, aim for regional anaesthesia extending T₁₀–S₄.

Other

Aminoglycoside antibiotics increase furosemide nephrotoxicity and potentiate non-depolarizing neuromuscular blockers.

NSAIDs impair production of prostaglandins (PGE₁) and prostacyclins (PGI₂), which modulate the vasoconstrictor effects of angiotensin II, noradrenaline and vasopressin. In the presence of renal disease or hypovolaemia, NSAIDs reduce renal blood flow and thus glomerular filtration rate. May worsen renal function or cause acute renal failure. May also cause oedema, heart failure and hypertension secondary to sodium retention.

Postoperative

Patient is usually extubated immediately postoperatively. Monitor CVP and renal function closely.

Common indications for renal transplantation

Anaesthesia for renal transplantation

Renal transplantation was first performed in 1906, but introduction of immunosuppressive drugs in the 1960s established this procedure as treatment of choice for end-stage renal failure. There are approximately 1800 renal transplants p.a. in the UK. Organ survival at 2 years is now 80% (cadaveric) – 90% (living donor); patient survival is 95%.

Dialyze pre-transplant to correct acid–base status and hyperkalaemia. Preoperative erythropoietin aims to maintain Hb 9.5 g.dL⁻¹, but may cause hypertension. Immunosuppressive drugs (cyclosporine, azathioprine, steroids, muromonab) may themselves cause morbidity. GA is usually the anaesthetic of choice as regional techniques risk bleeding and complicate assessment of intravascular volume. The kidney is usually transplanted into the right iliac fossa. Vascular anastomosis is performed prior to ureteric anastomosis. Avoid hypotension. If BP is low despite adequate filling (CVP ≥10–12 mmHg), consider low dose dopamine (<5 μg.kg⁻¹.min⁻¹). Vasoconstriction (α-effects) at higher rates may reduce renal blood flow, so change to dobutamine or dopexamine. Give diuretics to promote immediate renal function; mannitol may cause ↑ K⁺ and ↓↓ Na⁺ in renal failure. Avoid NSAIDs for postoperative analgesia.

Specific problems

Anaesthetic techniques

Both GA and spinal anaesthesia cause decreased BP and cardiac output after induction, with changes more marked with GA. Spinal anaesthesia is regarded as the technique of choice for TURP, although there are no proven difference in outcomes between GA and regional techniques.

General anaesthesia. Fit elderly patients can be managed with a laryngeal mask and spontaneous ventilation, but those with significant respiratory or cardiovascular disease are best managed by intubation and IPPV or regional technique.

Lithotomy position

Lithotomy position may result in hypoventilation and hypoxaemia due to a fall in FRC with age and supine position, and compression of lungs by abdominal contents. Thus, awake surgery may not be tolerated by all patients.

Lithotomy position increases the risk of gastric aspiration, particularly in obese patients and those with hiatus hernia. There is a further risk in the elderly due to impaired protective upper airway reflexes.

Increased CVP in the lithotomy position may cause angina or precipitate heart failure.

Bladder irrigation

Glycine 1.5% is slightly hypotonic (osmolality = 220 mOsm.L⁻¹). It is used because it is non-conductive, thus preventing dispersion of the diathermy current. Fluid absorbed through open venous sinuses in the prostate causes the TURP syndrome, characterized by:

Haemorrhage

Assess blood loss by measuring Hb in irrigation fluid collected from washout. Average blood loss is 500 mL.

Release of prostatic urokinase triggers conversion of plasminogen to plasmin with resulting fibrinolysis. This phenomenon may account for persistent bleeding in some patients. Plasminogen activators may be of benefit in extreme cases.

Bacteraemia

Urinary outflow obstruction predisposes to urinary tract infection. Prophylactic antibiotics are necessary if infection is present or if there is a risk of endocarditis.