Essential Notes for MRCS - Book 2(A)

Central mechanisms
Sometimes these central mechanisms are called the descending anti-nociceptive tract. The tract originates
in the periaqueductal grey and periventricular area of the midbrain, and descends to the dorsal horn of the
spinal cord; here enkephalins are released which cause presynaptic inhibition of incoming pain fibres.

Throughout the descending anti-nociceptive tract there are receptors that respond to morphine; the brain
has its own natural opiates known as endorphins and enkephalins which act along this pathway (opiate
analgesics act via these opioid receptors).

Spinal mechanisms
Opioids act directly at the spinal laminae inhibiting the release of substance P (the neurotransmitter
involved between the primary and secondary afferent fibres). This is the mechanism exploited by epidural
injection.

Mechanical inhibition of pain
Stimulation of mechanoreceptors in the area of the body where the pain originates can inhibit pain by
stimulation of large A fibres. (This is why analgesia is induced by rubbing the affected part or by applying
TENS.) TENS involves applying a small electrical current over the nerve distribution of the pain, which
activates the large sensory fibres and inhibits pain transmission through the dorsal horn. This is known as
‘pain gating’.

Perception of pain

This occurs in the thalamus and sensory cortex.

Referred pain
This is when pain is perceived to occur in a part of the body topographically distinct from the source of
the pain. Branches of visceral pain fibres synapse in the spinal cord with some of the same second-order
neurones that receive pain fibres from the skin. Therefore when the visceral pain fibres are stimulated,
pain signals from the viscera can be conducted through second-order neurones which normally conduct
pain signals from the skin. The person then perceives the pain as originating in the skin itself.

Visceral pain
Viscera have sensory receptors for no other modality of sensation except pain. Localised damage to
viscera rarely causes severe pain. Stimuli that cause diffuse stimulation of nerve endings in a viscus can
cause pain that is very severe (eg ischaemia, smooth muscle spasm, distension of a hollow viscus,
chemical damage to visceral surfaces).
Visceral pain from the thoracic and abdominal cavities is transmitted through sensory nerve fibres which
run in the sympathetic nerves – these fibres are C fibres (transmit burning/aching pain)
Some visceral pain fibres enter the spinal cord through the sacral parasympathetic nerves, including those
from distal colon, rectum and bladder
Note that visceral pain fibres may enter the cord via the cranial nerves (eg the glossopharyngeal and vagus
nerves) which transmit pain from the pharynx, trachea and upper oesophagus

If a disease affecting a viscus spreads to the parietal wall surrounding the viscera, the pain perceived will
be sharp and intense. The parietal wall is innervated from spinal nerves, including the fast A fibres.

Localisation of pain

Visceral pain is referred to various dermatomes on the body surface. The position on the surface of the
body to which pain is referred depends on the segment of the body from which the organ developed
embryologically, eg the heart originated in the neck and upper thorax, so the visceral pain fibres from the
surface of the heart enter the cord from C3 to T5. These are the dermatome segments in which cardiac
pain may be perceived. Pain from organs derived from the foregut is felt in the upper abdomen. Pain from
organs derived from the midgut is felt in the mid-abdomen, and pain from organs derived from the hindgut
is felt in the lower abdomen.

Parietal pain (eg from parietal peritoneum) is transmitted via spinal nerves which supply the external
body surface. A good example is acute appendicitis:
A colicky umbilical pain appears to ‘move’ to the right iliac fossa (RIF) and becomes constant • Visceral
pain is transmitted via the sympathetic chain at the level of T10; this pain is referred to the dermatome
corresponding to this area, ie around the umbilicus; this is colicky pain associated with obstruction of a
hollow viscus (the appendix)

When the inflamed appendix touches the parietal peritoneum, these impulses pass via spinal nerves to
level L1–2. This constant pain will be localised in the RIF (at McBurney’s point, a third of the distance
from anterosuperior iliac spine to the umbilicus).

Acute pain

Methods of assessing acute pain

Subjective measures of acute pain
Verbal scale:
• None
• Mild
• Moderate
• Severe
Visual analogue score:
• Ranging from worst pain ever (10) to no pain at all (0)
• Smiley faces, sad faces (for children)

Objective measures of acute pain
Most are indirect (eg blood pressure variations, vital capacity)

Inadequate analgesia
Inadequate post-op pain relief may be due to:
Expectation (of the patient, nursing staff or medical team)
Prescription method: prescribe prophylactically and regularly rather than on demand
Inability to use or intolerance of the pain relief method (eg if the patient is immobile, arthritic or confused
and so unable to use patient-controlled analgesia [PCA])

Harmful effects of undertreated acute pain

Cardiovascular effects
Tachycardia
Hypertension
Increased myocardial oxygen consumption

Respiratory effects
Splinting of the chest wall and therefore decreased lung volumes
Basal atelectasis

Gastrointestinal effects
Reduced gastric emptying and bowel movement

Genitourinary effects
Urinary retention

Musculoskeletal effects
Muscle spasm
Immobility (therefore increased risk of DVT)

Psychological effects
Anxiety
Fear
Sleeplessness

Neuroendocrine effects
Secretion of catecholamines and catabolic hormones, leading to increased metabolism and oxygen
consumption, which promotes sodium and water retention and hyperglycaemia

Management of postoperative pain
The realistic aim of pain relief is not to abolish pain completely, but to ensure that the patients are
comfortable and have return of function with a more rapid recovery and rehabilitation. Two fundamental
concepts prevail:

Preventing the development of pain is more effective than treating established pain – give pre-emptive
analgesia, before surgical trauma, with parenteral opioids, regional blocks or NSAIDs
It is difficult to produce safe, effective analgesia for major surgery with a single group of drugs
(monomodal therapy). Better analgesia is achieved with combinations of drugs that affect different parts
of the pain pathway (multimodal therapy) – usually a combination of local anaesthetics, opioids and
NSAIDs

Note that, if possible, the choice should be of the least painful incisions (eg lower abdominal or
transverse incisions).

Postoperative analgesia
Multimodal therapy
Use regular non-opioid analgesic initially (eg paracetamol or NSAID, if not contraindicated) for minor
surgery • Use regional or local analgesia techniques (eg epidural or peripheral nerve blocks); they are
especially effective in the immediate post-anaesthetic period
In major surgery, opioids will be needed as an addition to the above to enhance analgesia; they are
especially useful in the immediate postop period and are still the mainstay for routine postop pain relief.
IV opioids are preferred as dose delivery of IM injections is erratic and has greater complications • IV
opioids are best administered in the form of PCA

The acute pain service (APS)
Each hospital should have an acute pain service team who should be responsible for the day-to-day
management of patients with postop pain. This is a multidisciplinary team using medical, nursing and
pharmacological expertise. Anaesthetists have a major role to play, since they not only initiate
postoperative analgesic regimens such as PCA and epidural infusions, but also are very familiar with the
drugs and equipment. Protocols for the strict management of PCA and epidural regimens are essential.

Chronic pain

Chronic pain is pain that persists after a time period when it would be expected that healing were
complete.

The aetiology involves physical neural system rewiring and behavioural and psychosocial factors. It is
very difficult to manage and requires specialist knowledge (often an anaesthetic subspeciality).

Management strategies include:
Assessment of chronic pain states
Multimodal therapy
Pain clinics

Aetiology of chronic pain

Neural system rewiring
In chronic pain states, there are microscopic neural changes in the dorsal horn, spinal cord and brain.
Neural connections are altered, resulting in central plasticity. These changes result in a reduced pain
threshold, in which there is exaggerated local response to mildly painful stimulus termed ‘hyperalgesia’
or connection of mechanoreceptive neurones to pain pathways in which non-painful stimuli are perceived
as painful, resulting in allodynia. Examples of plasticity of the neural system are phantom limb pain and
the pain of peripheral neuropathy.

Behavioural and psychosocial issues
Depression or anxiety occurs in 58% of chronic pain patients and there is a higher than normal incidence
of personality disorder. Psychological issues may represent aetiological factors or occur as the sequelae
to an unpleasant condition.

Types of chronic pain
May be skeletal, spinal, joint, muscle or neuropathic (eg burning)
Commonly back pain and headaches

Assessment of chronic pain
History of injury, medication use and comorbid illness (physical and psychological)
Pain history (amount, duration, constant vs intermittent, description, eg shooting vs burning) • Identify
effects of condition on physical, psychological, social and financial aspects of the patient’s life to
establish functional status
Exclude a treatable underlying medical condition
Identify behaviour patterns that may respond to behaviour modification techniques
Identify realistic treatment goals and time course

Multimodal therapy for chronic pain
Functional rehabilitation (multidisciplinary team [MDT] approach – nurses, psychologists,
physiotherapists and occupational therapists) coordinated in the pain clinic
Medication:
• NSAIDs and moderate opioids, eg tramadol or codeine for flare-ups
• Long-acting opioids (eg morphine sulphate tablet [MST], transdermal fentanyl) for analgesia
maintenance • Antiepileptics (gabapentin, lamotrigine) and antidepressants (tricyclic antidepressants
[TCAs] or serotonin selective reuptake inhibitors [SSRIs]) for neuropathic pain

Pain in malignancy
Pain from malignancy is a combination of:
Neuropathic pain (due to invasion of nerves)
Nociception (due to tissue damage)

Management of malignant pain:
Follow the WHO analgesic ladder (may require opioid analgesia)
Aim for regular, oral medication
Regional blocks (eg coeliac plexus block)
Radiotherapy can provide pain relief
CT-guided stereotactic percutaneous destructive procedures

Pharmacology of pain

The WHO analgesic ladder
Step 1 Simple analgesics (paracetamol, NSAIDs)
Step 2 Compound analgesics (eg co-codamol, co-dydramol)
Step 3 Opiates (oral morphine remains drug of choice)



Routes for administration of analgesics

Oral Sublingual

Intramuscular Rectal

Intravenous Inhalational

Subcutaneous Epidural

Transdermal Spinal

Paracetamol
Mildly analgesic and antipyretic orally
Given intravenously, 1 g paracetamol has been shown to be as effective as 10 mg morphine

Side effects of paracetamol:
Overdose can cause liver damage and/or failure

Non-steroidal anti-inflammatory drugs
Examples: diclofenac, ibuprofen
Anti-inflammatory, analgesic and antipyretic actions
Mainly act peripherally but have some central action
Mechanism of action is by inhibition of the enzyme cyclo-oxygenase (this therefore inhibits synthesis of
prostaglandins which sensitise pain receptors to noxious stimuli)

Side effects of NSAIDs:
Prostaglandins are important in gastric mucus and bicarbonate production, so gastric irritation and peptic
ulceration may result if their production is inhibited (especially in elderly patients)
Nephrotoxicity: chronic use can cause interstitial nephritis, papillary necrosis and urothelial tumours •
Increased bleeding results from decreased platelet adhesiveness because of inhibition of thromboxane
production • Bronchospasm in patients with asthma (use should be avoided)
May cause gout (especially indomethacin)
May displace warfarin or other drugs from plasma proteins
Aspirin overdosage causes metabolic acidosis and respiratory alkalosis

Opioid analgesics
Examples: morphine, diamorphine, fentanyl
Cause analgesia, euphoria and anxiolysis
Act centrally and peripherally at opiate receptors
Three main types of receptor: mu (μ), kappa (κ) and delta (δ)

Side effects of opiates:
Central side effects of opiates:
• Respiratory depression (by acting on respiratory centre)
• Nausea and vomiting (by acting on chemoreceptor trigger zone)
• Hypotension, especially if hypovolaemic or if taking vasodilating drugs (common cause of
postoperative hypotension) • Miosis
• Tolerance and addiction
Peripheral side effects of opiates:
• Constipation
• Delayed gastric emptying
• Urinary retention
• Spasm of the sphincter of Oddi

• Pruritis

Routes of administration of opiates
Oral opioids:
• Codeine phosphate, tramadol, oral morphine sulphate solution
• Not useful immediately after major surgery because of nausea and vomiting and delayed gastric
emptying • Very useful after day-case surgery and 3–4 days after major surgery
Intramuscular opioids:
• Most common form of postop analgesia, even though they are ineffective in providing effective
analgesia in up to 40% of patients • There is a fivefold difference in peak plasma concentrations among
different patients after administration of a standard dose of morphine, with the time taken to reach these
levels varying by as much as sevenfold • The minimum effective analgesic concentration (MEAC) may
vary by up to fourfold between patients • The ‘standard’ dose is likely to be optimal for a minority of
patients
Intravenous opioids:
• Continuous infusion leads to effective analgesia, but with significant risk of respiratory depression •
PCA is the safest form
Epidural opioid analgesia (see below)
Slow-release oral opioids:
• MSTs have modified release over 12 hours (therefore given twice daily)
• To calculate dose: titrate oral dose required to provide relief, then divide total daily oral dose into two
daily MST doses • Always provide additional oral morphine sulphate solution when required for
breakthrough pain

Management of analgesia
Remember to work up the ladder toward opiates. There are often substitutions that can be made:
Paracetamol should be given regularly as a starting point
Non-opioids (eg aspirin, NSAIDs, paracetamol) can control bone pain
Co-codamol two tablets four times daily is equivalent to morphine 6–8 mg 4-hourly
The starting dose of morphine should be titrated to pain (eg 10 mg 4-hourly) unless the patient is elderly or
has hepatorenal impairment.
Transdermal fentanyl or alternative oral drugs (eg OxyNorm) are useful if tolerance is poor

With opiates, always prescribe:
Antiemetic for first 2 or 3 days
A laxative to prevent constipation

Patient-controlled analgesia

Now widely used for postoperative analgesia
Administered via a special microprocessor-controlled pump, connected to the patient via an intravenous
line, which is triggered by pressing a button in patient’s hand
A pre-set bolus of drug is delivered, and a timer prevents administration of another bolus for a specified
period (lock-out interval)

Advantages of PCA
Dose matches patient requirements
Decreased nurse workload
Painless (no IM injections)
Additional placebo effect from patient autonomy

Disadvantages of PCA
Technical error can be fatal (be very wary of background infusions)
Expense of equipment

Cautions in the use of PCA
A dedicated IV cannula should be used to ensure that the drug from the PCA does not accumulate
retrogradely • Monitor respiratory rate and level of sedation
Patient must be orientated and fully understand how to use the system for it to be effective; use may be
difficult for some patients (eg rheumatoid arthritis or learning difficulties)

Sedation

Sedation can also be used in critical care as an adjunct to analgesia

Aims of sedation
Relieve anxiety
Help synchronisation with the ventilator
Encourage natural sleep
Permit unpleasant procedures

Routes for sedation
Bolus dosing: prevents over-sedation but is inconvenient
Infusion: risk of over-sedation. Can be discontinued each day until rousable then restarted as necessary

Drugs for sedation
Benzodiazepines (eg midazolam): reduce anxiety and are amnesic. Can accumulate with infusions and are
inexpensive • Propofol: rapid elimination. Does not accumulate but is expensive (however, avoiding
increased length of stay due to over-sedation may offset cost). May cause hypotension

2.6 Intravenous drug delivery



In a nutshell ...

Venous access may be achieved:
Peripherally: by insertion of cannulas into peripheral veins of the extremities (includes venous cut-

down) • Centrally: by insertion of a cannula through the peripheral system into a central large-bore
vessel or direct cannulation of central vessels

Peripheral venous access

In most patients requiring venous access for IV medication or fluids, a peripheral vein is the appropriate
route. Peripheral venous cannulation may be a life-saving procedure in hypovolaemic shock.

Cannula sizes range from 12 G (the largest, for rapid infusion in hypovolaemia) to 24 G (the smallest, for
children).

Note that flow is proportional to r4 (where r is the radius of the lumen of the cannula). High flow requires
a large bore.

Indications and contraindications for peripheral access

Indications for peripheral venous access
Fluid/blood infusion
Blood sampling
Drug administration
Central venous line via peripheral route, eg percutaneous indwelling central catheter (PICC) line •
Peripheral venous feeding

Contraindications for peripheral venous access
Local sepsis
Puncture of potential arteriovenous fistula sites in haemodialysis patients

Complications of peripheral venous access
Infection (local or systemic introduction of pathogens)
Thrombophlebitis (usually chemical, eg erythromycin, cytotoxic agents)
Subcutaneous haematoma
Extravasation (may just cause oedema, but cytotoxic agents can cause considerable tissue damage) •
Accidental arterial cannulation

Common sites used for peripheral venous access

Dorsum of hand
Median basilic, median cephalic, basilic veins at antecubital fossa (avoid in haemodialysis patients) •
External jugular vein
Long saphenous vein at the ankle (avoid in patients with coronary artery disease)
Dorsum of foot
Scalp veins in infants or neonates

Venous cut-down

Patients in hypovolaemic shock often have collapsed peripheral veins, resulting in difficult cannulation. In
such circumstances rapid access can be gained by open cut-down onto a vein and cannulation. The most
common veins used for this are the antecubital veins and the long saphenous vein. Of the antecubital
veins, the median basilic vein is most commonly used. It is found 2 cm medial to the brachial artery.



Procedure box: Venous cut-down

Indications
IV access in cases of circulatory collapse when attempts to establish peripheral venous access have

failed • Useful in trauma and burns
Patient positioning
Supine, with medial side of the ankle exposed
Procedure
Prepare the ankle on the medial side with antiseptic and drapes
Infiltrate LA into the skin over the long saphenous vein (unless immediate access is required) • Make a
transverse incision 1–2 cm anterior to the medial malleolus
Using blunt dissection, isolate the vein and free it from surrounding tissue
Ligate the distal end of the mobilised vein
Pass a tie around the proximal aspect of the vein
Make a small transverse venotomy
Dilate this with closed haemostatic forceps
Insert a large-bore cannula and secure it with the proximal tie
Close the wound with interrupted sutures and apply a sterile dressing
Post-procedure
Standard wound care
Observe for infection
Complication
Haemorrhage due to lack of vascular control

Figure 3.29 Pe riphe ral ve nous acce s s – ve ins of the fore arm



Figure 3.30 Ve nous cut-down into long s aphe nous ve in

Central venous access

Central venous cannulation is a potentially dangerous procedure, particularly in a hypovolaemic patient,
and should be performed only by (or supervised by) an experienced practitioner.
Central venous catheters may reach the SVC or right atrium via the basilic, cephalic, subclavian, external
and internal jugular veins. The most common sites are the subclavian and internal jugular veins. Insertion
of catheters into the IVC via the long saphenous or femoral veins is associated with a high incidence of
DVT and PE and should be considered only as a last resort.
Catheters may be introduced with the ‘through cannula’ technique, whereby a short plastic cannula is first

introduced into the vein:
Needle introduced into vein
Cannula advanced over needle and needle withdrawn
Catheter inserted through cannula and cannula withdrawn

The Seldinger technique uses a flexible metal guidewire as an intermediate step to prevent the catheter
coiling up on itself inside the vein:
Needle introduced into vein
Guidewire advanced through needle and needle withdrawn
Catheter advanced over guidewire and guidewire withdrawn

Catheters may be Teflon or Silastic – Silastic catheters are more expensive, but induce less reaction, are
more flexible, and are most suitable for long-term central venous access. Wide-bore Silastic catheters
(single-, double- or triple-lumen) (eg Hickman) are suitable for long-term parenteral nutrition or
chemotherapy and are introduced percutaneously or surgically and the skin tunnelled (to reduce catheter-
related sepsis) to an exit site on the chest wall.

Central venous anatomy

Catheters are usually inserted percutaneously, but may be placed under direct vision after surgical
exposure of the vein.

The subclavian vein
The axillary vein continues as the subclavian vein as it crosses the outer border of the first rib behind the
clavicle, and it ends behind the sternoclavicular joint where it joins the internal jugular vein (IJV) to form
the brachiocephalic vein. It is closely related to the subclavian artery above and behind it and to the dome
of the pleura below and behind it. The thoracic duct enters the brachiocephalic vein at its origin on the
left and cannulation of the right side is therefore safer.

The internal jugular vein (IJV)
As the IJV runs down in the neck, it comes to lie lateral to the internal and common carotid arteries deep
to sternomastoid muscle and joins the subclavian vein to form the brachiocephalic vein behind the
sternoclavicular joint. The vein may be punctured from three sites: the posterior border of sternomastoid
muscle, the anterior border of sternomastoid muscle and near its lower end between the two heads of the
sternomastoid muscle; the first route is the most commonly used.

Insertion of central venous access


Procedure box: Central venous access

Indications
Fluid infusion
Drug infusion
Cytotoxic drugs which would damage peripheral veins
Inotropic drugs
TPN (hypertonic solution would damage peripheral veins)
Pacemaker electrode insertion
Monitoring of central pressures (eg CVP, pulmonary artery pressure)

Contraindications
Local sepsis
Severe coagulation disorders

Patient positioning
The patient should be supine, with arms by the side, head turned to the opposite side
Prepare all your equipment and only then place the patient head down, just before you start the

procedure
Procedure (Seldinger technique)
You will need:
Skin preparation
10 ml plain LA in a 10-ml syringe with a blue needle (22 G) attached
10 ml 0.9% saline in a 10-ml syringe with a green needle attached (you must be able to differentiate
between the syringe containing anaesthetic and the one containing saline)
10 ml 0.9% saline to flush the line at completion
A CVP line kit complete with large-bore needle, guidewire, dilator and CVP line
Small scalpel blade
Silk suture and fixative dressings
Sterile surgical drape
Sterile gown and gloves

Ultrasonography for identification of target vessel
Prepare the CVP line itself by opening all the taps on the three lumens and flushing the line through with

0.9% saline to remove the air
Close all the taps except the lumen that the guidewire will emerge through (commonly marked with a

brown bung) • Position the patient. Patients should be supine with a head-down tilt of 20–30° to
prevent air embolism and distension of the vein. Make sure that you have prepared all equipment
before tilting the patient, because critically ill patients may not tolerate this position for long periods.
The procedure should be performed under aseptic technique so glove and gown and drape the patient
with sterile drapes
After infiltration of LA, and using the syringe filled with saline, introduce the green needle through the
skin
Subclavian approach
Immediately below the junction of the lateral third and medial two-thirds of the clavicle; advance the tip
towards the suprasternal notch, ‘walking’ the needle tip along the undersurface of the clavicle
Internal jugular approach
Palpate the sternomastoid muscle and place the fingertips of your left hand on the pulsatile right carotid
artery. You can gently displace the artery medially as you introduce the needle at the midpoint of the
anterior border of sternomastoid. Direct the needle tip away from your fingers (protecting the artery)
and towards the ipsilateral right nipple of the patient. The needle should be angled at 30° to the skin
surface
Technique for line insertion for both approaches
Aspirate gently as the needle advances, until there is free aspiration of blood, indicating that the vein has
been entered. You now know the depth and location of the vein
Attach the syringe to the large-bore needle and follow the track of the green needle with the large-bore
needle until blood is aspirated easily
Leaving the large-bore needle in the vein, detach the syringe and advance the guidewire through the
needle (some kits allow the guidewire to be advanced through the syringe without its removal from the
needle), checking that it advances freely, with no obstruction; then remove the needle over the
guidewire, ensuring that control of the guidewire is maintained at all times
Make a small nick in the skin with a scalpel blade at the site of entry and dilate up the tract by passing
the dilator over the guidewire
Railroad the catheter over the guidewire (you must always hold on to the distal part of the guidewire by
the patient’s neck until the proximal end emerges from the lumen of the catheter)
Check that the catheter advances freely with no obstruction, to its required length (approximately 20 cm)
• Remove the guidewire, suture the catheter to the adjacent skin and check that blood can be aspirated
freely from all lumens. Flush the line with 0.9% saline
Post-procedure
Take a chest radiograph in expiration to exclude a pneumothorax and to check the catheter tip is in the
optimal position (SVC or right atrium)
Complications of central venous catheterisation
Complications of insertion
Pneumothorax
Haemothorax (due to laceration of intrathoracic vein wall)
Puncture of adjacent artery causing subcutaneous haematoma, arteriovenous fistula or aneurysm •
Thoracic duct injury
Brachial plexus damage
Cardiac complications (arrhythmias, perforation of right atrium)

Malposition of the catheter (eg into neck veins, axillary vein or contralateral veins)
Complications of use

Catheter-related sepsis
Catheter occlusion
Catheter embolisation (due to migration of detached catheter)
Central vein thrombosis

Subcutaneously implanted vascular access systems

These consist of a stainless steel (Port-a-Cath) or plastic (Infuse-a-Port) reservoir with a silicone septum
buried in a subcutaneous pocket and connected to a Silastic central venous catheter. Access to the
reservoir is with a percutaneous needle, which pierces the self-sealing septum without coring. Used for
long-term antibiotics or chemotherapy.

Intraosseous puncture

This is an emergency technique for fluid resuscitation.


Procedure box: Intraosseous puncture

Indication
Used in emergency situations in children aged 6 years or younger in whom venous access by other means

has failed on two attempts.
Contraindications
Local sepsis
Ipsilateral fractured extremity
Complications
Misplacement of the needle (this usually involves incomplete penetration of the anterior cortex or over-
penetration, with the needle passing through the posterior cortex)
Epiphyseal plate damage
Local sepsis
Osteomyelitis
Technique of intraosseous puncture
Identify the puncture site – approximately 1.5 cm below the tibial tuberosity on the anteromedial surface
of the tibia • Clean and drape the area
If the patient is awake infiltrate the area with LA
Direct the intraosseous needle at 90° to the anteromedial surface of the tibia
Aspirate bone marrow to confirm the position
Inject with saline to expel any clot and again confirm the position; if the saline flushes easily with no
swelling the needle is correctly placed
Connect the needle to a giving set and apply a sterile dressing
Post-procedure
Discontinue as soon as reliable venous access has been established

Infuse and pump



In a nutshell ...

The principles of cardiovascular support in circulatory failure follow the VIP rule:
Ventilate
Infuse
Pump

The ventilatory support has been covered earlier, intravenous access has been achieved, so now the
‘infuse and pump’ principle aims to maximise blood flow and perfusion to vital organs by means of:
Appropriate fluid management
Drugs

Infuse

Fluid challenge using invasive monitoring
Use of colloids as tighter dose response relationship
Always ensure adequate filling before vasoactive support (Starling’s)



Fluids: the crystalloid–colloid controversy
Crystalloids
Consist of salt ions in water
Of the volume infused, about a third stays intravascular and two-thirds pass to ECF, hence risk of tissue
oedema • Examples: 0.9% sodium chloride, Hartmann’s solution
Advantage: ECF fluid deficit in shock is replaced
Colloids
Consist of osmotically active particles in solution
Expand plasma volume by volume infused
May leak into interstitium in capillary leak syndrome
Examples: gelofusine, Haemaccel (gelatine-based, half-life about 4 hours)
Dextrans (degraded dextrose; interfere with cross-matching)
Starches (long half-life in some cases; 10% solutions hyperoncotic hence increase plasma volume more
than volume infused; some may have benefit in reducing capillary leak syndrome)
Albumin (pasteurised; suppresses albumin synthesis; normally some albumin leaks through the capillary
membrane) • Blood (plasma-reduced has haematocrit of about 70%)

A combination of crystalloids and colloids is probably the best approach.

Dextrose-containing fluids are not useful for intravascular volume replacement because they only replace
water, which, as the sugar is metabolised, redistributes to intracellular and extracellular compartments.
The dextrose allows water to be isotonic for IV infusion.

Potassium is replaced at a maximum rate of 20 mmol/hour in a monitored ITU environment. In
hypokalaemic patients this reflects a large total intracellular deficit.

Magnesium replacement should be considered, aiming for a serum level of 1 mmol/l.

Volume-expanding fluids should be considered separately from maintenance fluids. See section 1.3 of this
chapter for further detail on maintenance of fluid balance.

Pump

The first priority in shock of any cause is to restore perfusion pressure; the second is to optimise cardiac
output.

Blood pressure
Aim for MAP >60 mmHg or systolic BP >90 mmHg (elderly people often require higher pressure to
perfuse vital organs due to pre-existing hypertension)
An adequate perfusion pressure should maintain urine flow
If systemic vascular resistance (SVR) is low then a vasopressor such as noradrenaline is indicated to
improve perfusion pressure once normovolaemia has been reached
Vasoconstriction may mask hypovolaemia, so closely monitor filling pressures and cardiac output,
especially during inotropic infusion

Cardiac output
Drugs may be used to increase cardiac output by positive inotropic effect or increase perfusion to a
specific organ system (eg renal and mesenteric blood flow is increased by dopexamine infusion at a rate
of 0.5–1 μg/kg per minute; no evidence for prevention of renal failure) • Monitor effect via DO2, lactate,
pH, urine output, cardiac output • Adrenaline: inotrope, vasopressor, chronotrope. Activates β receptors,
increasing intracellular cAMP. At low dose it has β effects mostly, and as doses increase has greater
effect on α receptors; β2 effects cause vasodilatation in skeletal muscle beds, lowering SVR
Dobutamine: inotrope, vasodilator, synthetic. Predominant β1 effect increases heart rate and force of
contraction, and hence cardiac output. Mild β2 and α effects overall, causing vasodilatation
Dopamine: up to 5 μg/kg per minute has dopamine receptor activity causing renal dilatation; 5–10 μg has
mostly a β-inotropic effect. Above 15 μg has mostly an α-vasoconstrictive effect. Unpredictable ranges in
different patients. Problems with dopamine include: gut ischaemia, growth hormone suppression,
immunosuppression
Dopexamine: mesenteric and renal vasodilatation via dopamine receptors, and also has β2 effects.
Synthetic. Anti-inflammatory effect. May protect the gut against ischaemia in the presence of
vasoconstrictors. Used at a dose of 0.5–0.9 mg/kg per minute for mesenteric protection • Noradrenaline:
vasopressor effect predominates. Mild inotropic β1. Increases SVR to improve perfusion pressure but
may suppress end-organ and skin perfusion due to capillary vasoconstriction. Used to increase perfusion
pressure in septic shock • Isoprenaline: chronotrope used to increase heart rate in heart block while
awaiting pacing; β1and β2 effects
Phosphodiesterase inhibitors: milrinone, enoximone. Increase intracellular cAMP by decreasing its
breakdown. Increase inotropic and vasodilatation (inodilator and lusiotropic). Increased cardiac output,
lowered pulmonary artery occlusion pressure and SVR, but no significant rise in heart rate or myocardial
oxygen consumption
Hydralazine: mostly arterial vasodilatation; to control BP
Nitroprusside: arterial vasodilator with short half-life given as infusion • Nitrates: venodilators, reducing
pre-load



Cardiac drugs
Inotropes: increase force of ventricular contraction (usually a β effect) • Lusiotropes: enhance

myocardial relaxation
Vasopressors: vasoconstrict blood vessels (α effect)
Vasodilators: vasodilate blood vessels (arterial, venous or both) • Chronotropes: increase heart rate (β

effect)
Usually infused in micrograms per kilogram per minute. Dose ranges and individual effects are
unpredictable in the critically ill patient.

SECTION 3

Postoperative complications

3.1 General surgical complications



In a nutshell ...

Postoperative complications may be classified by time of occurrence:
Immediate
Early
Late

They may also be classified according to their underlying cause:
General complications of surgery

• Haemorrhage
• Pyrexia
• Venous thromboembolism
• Wound complications and surgical site infection
Complications specific to the operation:
• Anastomotic leak after bowel resection
• Infection of prosthetic material after joint replacement • Hypocalcaemia after parathyroid surgery
Complications related to patient comorbidity
• Can affect any system: cardiac, respiratory, GU, GI, neurological

Risk factors for postoperative complications

Extremes of age
Obesity
Cardiovascular disease
Respiratory disease
Diabetes mellitus
Liver disease
Renal disorders
Steroids and immunosuppressant drugs

Complications may be immediate, early or late and may also be specific to the operation or general to any
operation.
Immediate complications occur within 24 hours of surgery • Early complications occur within the 30-day
period after the operation or during the period of hospital stay • Late complications occur after the
patient has been discharged from hospital or more than 30 days after the operation



Remember:
Prophylaxis
Early recognition
Early management

General complications of surgery

Haemorrhage

Primary haemorrhage occurs during the operation; it should be controlled before the end of the operation
• Reactionary haemorrhage occurs usually in the first few hours after surgery, eg clot disturbance with
raised BP
Secondary haemorrhage occurs a number of days after the operation; the cause is usually infection-
related, but can also be related to sloughing of a clot or erosion of a ligature

Predisposing factors for haemorrhage
Obesity
Steroid therapy
Jaundice
Recent transfusion of stored blood
Disorders of coagulation
Platelet deficiencies
Anticoagulation therapy
Old age
Severe sepsis with DIC

Prevention of haemorrhage
Recognise patients at risk
Reverse risk factors if possible
Liaise with haematologist about managing coagulative disorders • Control of infection
Meticulous surgical technique

Management of haemorrhage
Resuscitate
Correct coagulopathy
Consider blood transfusion
Surgical or interventional radiology haemostasis if necessary • Packing may be necessary

Postoperative pyrexia

Pyrexia is a common complication. Consider:
Is it a correct measurement?
How was the temperature measured?

What is the trend?
New onset?
Persistent elevation?
‘Swinging’?

Is it due to an infection?
DVT and PE can present with low-grade pyrexia
Compartment syndrome may cause pyrexia
Early pyrexia may be a response to surgical trauma or blood transfusion

Is there evidence of systemic involvement?
Rigors
Shivering
Sweating

Is it related to drugs or infusions?
Allergy
Blood transfusion reaction
Gelofusine can cause reactions

Recent culture results?
Tailor the correct antibiotic specific to the bacteria grown

Different causes tend to manifest at different time points in the postoperative period. However, these are
not absolute and you should consider all causes.



Postoperative pyrexia
Day 1–3
Atelectasis
Metabolic response to trauma
Drug reactions (including to IV fluids)
SIRS
Line infection
Instrumentation of a viscus or tract causing transient bacteraemia
Day 4–6
Chest infection
Superficial wound infection
Urinary infection

Line infection
Day 7 onwards

Chest infection
Suppurative wound infection
Anastomotic leak
Deep abscess
DVT

Investigation of a postop pyrexia
Bloods, including WCC, neutrophil count and CRP
Septic screen
Blood for culture (take from peripheral site and a separate sample through any potentially infected line; if
removing lines send line tips for culture)
Urinalysis
Wound swab
Sputum culture
Stool culture (eg antibiotic-associated colitis)
Tailor special investigations to examination findings (eg chest radiograph for respiratory symptoms or
signs; abdominal CT to look for deep abscess)

Note: in the 24 hours after surgery, CRP will almost always be raised due to trauma and so should not be
measured routinely; an upward trend in CRP measurements is a sensitive marker of infection (CRP
increases within 24 hours of an insult).

Wound complications



Risk factors for wound complications
Type of operation
Potentially contaminated operations (eg elective operations on GI tract) • Contaminated operations (eg

perforated duodenal ulcer)
Dirty operations (eg faecal peritonitis)
Obesity
Haematoma
Diabetes
Steroids
Immunosuppression
Malnutrition
Obstructive jaundice
Foreign material
Vascular grafts
Joint replacements
Heart valves
Hernia mesh

Note that the effects of infection in cases with implanted prosthetic material can be devastating.

Prophylaxis for wound infections
Identify patients at risk
Reduce/control risk factors
Meticulous surgical technique
Antibiotic prophylaxis
Bowel preparation

Treatment of wound complications

Wound infections
Ensure adequate drainage
Send fluid/pus for culture and sensitivity
Debride if necessary
Appropriate dressings
Antibiotics only if acute infection (cellulitis, septic)
Dehiscence requires urgent surgical repair

Abscesses
Drain – radiological, surgical
Treat underlying cause (eg anastomotic leak)

Septicaemia/septic shock
Early recognition
Treat and/or remove source of sepsis
Organ support as required on HDU/ITU

Complications of specific surgery

Complications of GI surgery

Anastomotic haemorrhage or leak (± peritonitis or abscess) • Visceral injury (due to adhesions)
Ileus
Oesophageal surgery: reflux, fungal infections, strictures • Gastric surgery: ‘dumping syndrome’, nausea,
pancreatitis • Biliary surgery: leaks, bile duct injuries, strictures
Small-bowel surgery: short-gut syndrome, malabsorption
Colorectal surgery: stoma formation, anastomotic leaks, wound infection

Complications of vascular surgery

Carotid surgery
TIA/CVA
Hyperperfusion syndrome
Patch dehiscence and secondary haemorrhage

Cranial nerve injuries

AAA repair
Damage to adjacent structures (eg left renal vein)
Prosthetic infection
Acute ischaemic colitis
Retroperitoneal haematoma
Impotence
Spinal ischaemia (in thoracic aneurysmal procedures)
Endoleaks and stent migration (for endovascular aneurysm repair procedures)

Arterial by-pass grafting
Anastomotic leaks or rupture
Graft thrombosis and failure (± amputation)
False aneurysm formation
Compartment syndrome
Disease progression
Graft infection

Venous surgery
Damage to nerves (saphenous and sural)
DVT
Major venous injury (to femoral vein)
Recurrence

Complications of cardiothoracic surgery

Cardiac surgery
Arrhythmia
Anastomotic bleeding/blow-out
Low cardiac output
MI

Pulmonary surgery
Persistent air leak
Atelectasis
Bronchopleural fistula
Empyema

Complications of orthopaedic surgery
Prosthetic infection
Joint dislocation

Periprosthetic fracture
Malunion
Non-union
DVT

Complications of urological surgery

Renal surgery
Haemorrhage
Arteriovenous fistula
Urinary leaks

Ureteric surgery
Stenosis
Obstruction
Hydronephrosis

Bladder surgery
Ileus
Rectal injury

Complications of plastic surgery

Unsightly scarring
Flap failure and necrosis

Complications of breast surgery

Damage to axillary structures
Seroma, haematoma and wound infection
Lymphoedema and limited movement of arm
Nerve damage
Breast deformity

Rehabilitation

For surgeons the ultimate goal is success of surgery. However, this does not just mean getting patients off
the operating table; it includes postoperative care and rehabilitation during that time, and eventually
getting the patient successfully back into the community with any adjustments and help that are necessary.
What is the physical injury or operation?
What is the likely outcome and effect on physical status?
What is the existing home/work situation?

Things to consider include:

Multidisiplinary team (MDT) input
Communication with:
• Patient
• Relatives
• Nurses
• Physiotherapists
• Occupational therapists
• Social services
Transfer possibilities:
• Home (± increased level of care)
• Increased level of care (residential home or nursing home) • Hospice
• Rehabilitation unit

Specific rehabilitation needs

Some injuries or procedures have specific rehabilitation needs, eg:
Multiple trauma
Head injuries
Stoma patients
Amputation
Mastectomy
Transplant recipients

Consider the following:
Age and pre-hospital function
Understanding and acceptance of injuries
Long-term analgesia requirements
Goal setting (ideal vs realistic)
Early physiotherapy
Occupational therapy (time frame)
Employment and income issues
• If self-employed:
• More likely to want to restart work early, whether their rehab is complete or not • Family need money
• If company-employed:
• Sick pay
• Stigma of ‘being on the sick’
Psychological issues
• Psychiatric review
• Social worker
• Support groups

3.2 Respiratory failure

Postoperative respiratory complications

In a nutshell ...

Respiratory problems are very common following surgery. Risk factors include:
Patient factors
Anaesthetic factors
Perioperative factors
Trauma

The management of respiratory problems is covered earlier in this chapter.

Risk factors for respiratory problems

Patient factors
Age
Pre-existing respiratory disease
Smoking
Obesity
Pre-existing cardiac disease
Immobility
Postoperative pain

Anaesthetic factors
Reduced residual capacity resulting from supine position and raising of diaphragm • Ventilation–perfusion
mismatching: increased shunt – perfused but not ventilated; increased dead space – ventilated but not
perfused
One-lung ventilation
Excessive sedation
Residual anaesthetic agents (muscle relaxants)
Impaired host defences: impaired protective reflexes (eg gag and cough); dry anaesthetic gases hinder
ciliary function

Perioperative factors
Upper abdominal/thoracic wounds
Analgesia/sedatives (eg opiates)
Pain restricting respiratory effort and adequate cough
Lying supine

Trauma factors
Cord lesions
Analgesia
Pain
Rib fractures/resection
Pneumothorax
Lung contusion

Common respiratory postoperative pathology

Basal atelectasis (most common)
Bronchopneumonia
PE
Pleural effusion
Pneumothorax
Respiratory failure
ARDS/acute lung injury

Investigating postop respiratory problems

Chest radiograph
ABGs (see earlier for interpretation of ABGs)
ECG to exclude cardiac cause

Management of postop respiratory problems

Risk factors corrected before surgery
Adequate postoperative analgesia (epidural is ideal for major abdominal surgery) • Minimal sedation
Early and regular physiotherapy
Early mobilisation
Antibiotics if evidence of infection
Drainage of effusion/pneumothorax
Ventilatory support if necessary

3.3 Acute renal failure

Renal physiology



In a nutshell ...

The kidney has multiple functions.
Homeostasis of the extracellular fluid: control of water and electrolyte balance by plasma filtration
followed by excretion and resorption of ions and water.
Excretion: elimination of waste products of metabolism (eg ammonium-containing compounds) and
foreign substances (eg drugs).
Metabolism: vitamin D hydroxylation and activation.
Endocrine: production of erythropoietin and control of the renin–angiotensin–aldosterone system.

Renal blood flow

The kidneys receive 20–25% of the cardiac output, ie approximately 1200 ml/min, yet only represent
0.5% of the body mass. This is called the renal fraction. The kidneys contribute to local control of renal
blood flow by production of several hormones (eg renin, prostaglandins, nitric oxide and the kallikrein

cascade).
Factors influencing renal blood flow include:
Increased flow:
• Hormones (ANP)
• Drugs (dopamine, dobutamine, captopril, furosemide)
Decreased flow:
• Hormones (ADH, renin)
• Anatomy (renal artery stenosis)
• Drugs (β blockers, indomethacin)



Figure 3.31 The s tructure of the ne phron



Figure 3.32 The vas culature s urrounding the ne phron

The nephron

Each kidney has about 1 million functional units or nephrons arranged in parallel (Figure 3.31). The
nephron has two main regions – the glomerulus and the tubule. The glomerulus handles blood flow to the
kidney and initial plasma filtration. The tubule further filters and processes the filtrate, reabsorbing water