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Chapter 3 Drug calculations and numeracy skills

We hope these examples have helped you to

understand the processes involved in bolus dose

calculations over time.

Drug calculations by weight

Some medications require us to calculate the dose

based on a patient’s weight. These drugs are pre-

scribed on a mg per kg basis and therefore we

must obtain the patient’s weight in kilograms.

Many of these calculations are for medication for

children and it is essential we get the doses cor-

rect, as errors can lead to overdose and compli-

cations. Here is an example to illustrate the point:

Example 1

Your patient requires their medicine at a dose

of 60mg/kg/day (milligrams per kilogram per

day). The patient weighs 12kg.

So the calculation will look like this:

60 × 12 = 720mg per day

This might be a one-off dose or it may be

required to be split. Let’s say we want to give it

in 4 divided doses, thus:

720 / 4 = 180mg per dose

Can you see how that worked? Here are some others:

Example 2

Your patient requires their medicine at a dose of

30mg/kg/day.

The patient weighs 15kg.

The dose must be given in 3 divided doses.

So the calculation will look like this:

30 × 15 = 450mg per day

450 / 3 = 150mg per dose

When a dose calculation by weight needs to be

made for a child, a liquid dose calculation might

also need to be made. Here are all the steps

involved:

Example 3

Your patient requires their medicine at a dose of

50mg/kg/day.

The child weighs 20kg.

The drug must be given in 4 divided doses.

You have a liquid available that is 125mg in 5mL.

So the calculation will look like this:

50 × 20 = 1000mg per day

1000 / 4 = 250mg per dose

250 / 125 × 5 = 10mL per dose

We hope that you are now clear about making

weight calculations.

You should now be in a position to attempt the

practice calculation questions at the end of this

and the other chapters in the book. Have a look

at the case studies below where drug calcula-

tions would be needed for the proper delivery of

medication.

Case studies

James Jones is 4 years old and has a fever. His doctor has prescribed paracetamol to

help reduce his temperature and wants it given at a dose of 60mg per kg per day, but it must be

divided into 4 doses and not given all at once. James has been weighed on admission and he is

16kg. Work out how much paracetamol he can have per day and how much he can have if this

must be divided into 4 doses.

With this chapter in mind, outline which mathematical processes you would have to use and

which drug calculations you would need to perform. Reflect on the impor tance of getting this

calculation correct.

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Chapter 3 Drug calculations and numeracy skills

Helen Taylor is admitted for surgery and requires a bolus dose of antibiotic before theatre. She

is prescribed 300mg of Ciprofloxacin by intravenous infusion over 60 minutes. The dose must be

prepared, and you have a 200mL bottle containing 2mg per mL. How many mL from the bottle

is required to give 300mg and how much will be left in the bottle? If this dose is to be given as

prescribed, at what rate does it need to be delivered over 60 minutes?

With this chapter in mind, outline which mathematical processes you would have to use and

which drug calculations you would need to perform. Reflect on the impor tance of getting this

calculation correct.

Key learning points

▶

Numeracy is integral to safe nursing practice.

▶

The ability to use basic principles such as addition, subtraction, multiplication and division

is paramount in health care.

▶

The ability to convert between units of mass lays the foundations for drug calculations.

▶

The ability to calculate doses in solid and liquid form is essential, as is the ability to calculate

drug administration over time and by weight.

Answers to questions in this chapter

Addition Subtraction

11 + 27 = 38

23 + 45 = 68

101 + 273 = 374

450 + 339 = 789

1022 + 2174 = 3196

19 − 17 = 2

53 − 41 = 12

177 − 73 = 104

458 − 334 = 124

1726 − 1114 = 612

Multiplication Division

3 × 4 = 12

9 × 7 = 63

10 × 3 = 30

20 × 4 = 80

6 × 15 = 90

12 / 4 = 3

150 / 3 = 50

500 / 2 = 250

20 / 4 = 5

600 / 5 = 120

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Chapter 3 Drug calculations and numeracy skills

Recommended further reading

Local anaesthetics and

analgesics

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Chapter 4 Local anaesthetics and analgesics

Introduction

Pain is a sensation that lets us know about dam-

age to our tissues. It is one of our normal defence

mechanisms and is important to our survival.

Therefore, when we consider modifying the expe-

rience of pain, it is important to remember that,

although distressing and unpleasant, pain has a

role to play in protecting us. It is possible to suffer

severe pain without any obvious tissue damage or

injury, such as trigeminal neuralgia (severe burn-

ing or stabbing pain in the face arising from one of

the nerves carrying sensation). On the other hand,

pain may become a dominant feature in a person’s

life long after tissues have healed, such as phan-

tom limb pain. It is also possible that tissue dam-

age in one part of the body can lead to pain being

perceived in another part of the body, something

that is called referred pain.

Pain is therefore a difficult concept to define. As

it becomes more chronic in nature (i.e. more than 6

months in duration), it begins to affect all activities

of daily living, not just from a physical but also from

a psychological and sociological perspective. The

nurse has a unique role to play in minimizing pain

for patients. To carry out this role effectively, nurses

need to have some understanding of the drugs used

in pain relief. The NMC Standards of Proficiency for

Registered Nurses (NMC 2018) state:

Platform 4: Providing and evaluating care

4.8 demonstrate the knowledge and skills

required to identify and initiate appropriate

interventions to support people with commonly

encountered symptoms including anxiety, con-

fusion, discomfort and pain

We first need to remind ourselves of the basic prin-

ciples of the initiation and conduction of nerve

impulses and the body’s pain pathways and analge-

sic system.

Neurones

Neurones are specialized cells in the nervous sys-

tem whose function is to transmit messages. A neu-

rone has branch-like processes called dendrites

that convey incoming messages (action potentials)

towards the cell body (see Figure 4.1). The cell body

houses the nucleus and therefore is the metabolic

centre. Structures known as axons, which terminate

in axon terminals, conduct impulses away from

the cell body. Housed in the axon terminals are hun-

dreds of small sacs (vesicles), which contain neu-

rotransmitters. The nerve impulse therefore travels

from the dendrites along the axon and finishes at

the axon terminal where the impulse stimulates the

release of the neurotransmitter.

Several neurones are covered with a substance

called myelin, formed by supporting cells called

Schwann cells, which wrap themselves around the

axon. The myelin covering acts as an insulator for

the nerve and affects the speed at which messages

can travel along individual neurones.

Neurones carrying messages from the internal

organs and skin into the central nervous system

are called sensory (afferent) neurones. Conversely,

neurones carrying messages out of the central

■ Name at least two major drugs from the non-steroidal anti-inflammatory and opioid classifi-

cations of analgesics.

■ Compare the mode of action of non-steroidal anti-inflammatory and opioid analgesics.

■ Demonstrate knowledge of the unwanted effects of non-steroidal anti-inflammatory and opioid

classifications of analgesics.

■ State the major opioid antagonist used in clinical practice.

■ Define the term ‘adjuvant drug’.

■ Outline the use of novel analgesics in neuropathic pain

■ Correctly solve several drug calculations about local anaesthetics and analgesic drugs.

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Chapter 4 Local anaesthetics and analgesics

nervous system to the muscles, glands and internal

organs are called motor (efferent) neurones.

The nerve impulse

At rest, the inside of a neurone has a negative

charge compared to the outside, which is positive.

This is because the inside of a neurone carries a lot

of negatively charged particles called anions. Ani-

ons are large particles that have difficulty moving

through the wall of the neurone. In contrast, the

outside of the neurone contains lots of positively

charged particles called cations. The major cation

in our discussion here is sodium.

To trigger the sensation of pain, the inside of the

neurone must become positively charged. A nocic-

eptive stimulus can cause chemicals to be released

by damaged tissue (examples of these include

bradykinin, histamine, serotonin, potassium and

other proteolytic enzymes), which in turn can

bring about a change in the neuronal membrane,

allowing sodium to pass into the neurone. As

the sodium enters, the membrane becomes even

more permeable to sodium. This continues until

the inside of the neurone is positively charged in

relation to the outside. This build-up of positively

charged sodium is termed depolarization.

At the synapse, where one neurone meets

another, neurotransmitters must be released to

stimulate the next neurone to continue to pass the

message onwards. This process is important when

considering analgesics and how they work. Once

the neurone has converted to a positive environ-

ment, calcium channels in the membrane open, so

allowing calcium to enter. The influx of calcium

attracts small sacs called synaptic vesicles, which

are full of neurotransmitters, towards the synapse.

When these vesicles reach the synapse, they fuse

with the neurone membrane and release the neuro-

transmitter into the synapse itself (see Figure 4.2).

The neurotransmitters that are important in

the pain pathway are substance P, neurokinin A

and B, and glutamate. Once the neurotransmitter

attaches itself to receptors on the other side of the

synapse, this neurone then becomes permeable to

sodium and the process continues (see Figure 4.3).

Having discussed the initiation and transmission

of a nerve impulse, we need now to consider the

body’s pain pathways.

Cell body

Dendrites

Nucleus

Myelin

Node of Ranvier

Axon body

Synaptic

terminals

Figure 4.1 A neurone

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Chapter 4 Local anaesthetics and analgesics

Pain reception

Pain is received via specialist receptors called

nociceptors, which are free nerve endings that lie

in the tissues. They are most plentiful in the skin;

as you move deeper into the tissues of the body,

they become fewer in number. Nociceptors can be

stimulated by mechanical, thermal and chemical

means and have a high threshold. This means

that only stimuli indicating some degree of tissue

damage are perceived as pain. Nociceptors are non-

adapting, which means they are stimulated at the

same level of intensity each time the threshold level

is reached. In other words, you do not raise the

threshold at which the nociceptors are stimulated

Figure 4.2 Firing of a neurone

DENDRITES

SODIUM MOVES INTO

NEURONE

++++++++++

––––––––––

INSIDE OF NEURONE

IS NOW POSITIVE

Region of depolarization

Resting state re-established

Cell body

Resting state Axon

Direction of impulse movement

SYNAPTIC KNOB

BECOMES POSITIVE

CALCIUM MOVES

INTO NEURONE

NEUROTRANSMITTER

RELEASED INTO SYNAPSE

VESICLES CONTAINING

NEURONE TRANSMITTERS FUSE

WITH SYNAPTIC NEURONE

–––+

++++++

–––+

++++++

+++–

––––––

+++–

––––––

+++–––

++++

+++–––

++++

–––+++

––––

–––+++

––––

++++++––

–+

++++++––

–+

––––––++

+–

––––––++

+–

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Chapter 4 Local anaesthetics and analgesics

just because the pain is constant. This is an impor-

tant aspect to our survival.

In addition to noxious stimuli like heat and

pressure, nociceptors can become sensitive to a

variety of chemicals that are present after local

tissue injury. These substances include potassium,

serotonin, bradykinin, histamine and prostaglan-

dins. Prostaglandins are normally produced by the

body to ensure the smooth running of our internal

environment (homeostasis). They are especially

important in the case of certain medicines, such

as NSAIDs.

Painful stimuli are received by the nociceptors

and then transmitted by two different types of

nerve fibres: A-delta fibres and C fibres. A-delta

fibres are myelinated fibres, small in diameter,

which are stimulated by mechanical means. A mye-

linated nerve is one covered by a fatty insulating

substance called myelin. As the fibres are myeli-

nated, they convey impulses very quickly. Stimu-

lation of these fibres leads to sharp prickling pain

that the person can easily localize. C fibres are

also fibres of small diameter but are unmyelinated

and so convey impulses more slowly, resulting in

a ‘burning’ or ‘aching’ pain that is harder to pin-

point. It will tend to be more general in nature, and

a good example is abdominal pain.

Both A-delta and C fibres synapse with the next

neurone in the pathway in the dorsal horn of the

spinal cord. It is in this area of the dorsal horn (i.e.

the substantia gelatinosa) that Melzack and Wall

(1965) proposed a gate-controlled entry for the

sensation of pain into the central nervous system.

If the gate is opened a person will perceive pain,

whereas if the gate is closed they will not.

The sensation of pain is then carried by what

are referred to as the spinothalamic tracks, which

carry impulses from the spinal cord up to the thal-

amus. One track carries information from the

A-delta fibres and the other from the C fibres.

These tracks once again synapse in the thalamus

and the impulses are conveyed to several areas,

including the sensory cortex, where they are inter-

preted as pain (see Figures 4.4 and 4.5).

Figure 4.3 Transmission of a nerve impulse

Axon

Nerve impulse

Pre-synaptic

neurone

Vesicle

Transporter

Neurotransmitter

Receptors

Post-synaptic

neurone

Synaptic space

Dendrite

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Chapter 4 Local anaesthetics and analgesics

Somatosensory

cortex

Thalamus

Brainstem

Cerebellum

Spinal cord

Afferent nerve fibre fro

pain or temperature

receptor

Spinal cord

(transverse

section)

Figure 4.4 Spinothalamic tracks

Figure 4.5 Ascending pain pathways

SOMATOSENSORY,

LIMBIC AND FRONTAL

AREAS OF THE BRAIN

THALAMUS

NEOSPINOTHALAMIC

PATHWAY

A-DELTA

FIBRES

PALEOSPINOTHALAMIC

PATHWAY

C FIBRES

DORSAL HORN

OF SPINAL CORD

NOCICEPTORS

STIMULATED

PERIAQUEDUCTAL

GREY (PAG)

NUCLEUS RAPHE MAGNUS

(NRM)

DORSAL HORN

OF SPINAL CORD

SOMATOSENSORY,

LIMBIC AND FRONTAL

AREAS OF THE BRAIN

ENDORPHINS DYNORPHINSENKEPHALINS

Figure 4.6 Descending pain pathways

The body’s analgesic system

As with other sensory systems in the body, the

pain pathway has a descending mechanism (see

Figure 4.6). This mechanism constitutes the body’s

attempt to modify the pain we interpret. In other

words, it is our inbuilt analgesic system.

This analgesic system commences at an area of

the brain called the periaqueductal grey (PAG). This

is a tiny part of grey matter that lies in the mid-brain.

It receives input from several brain areas, among

them the hypothalamus, cortex and thalamus.

The PAG is thought to be the mechanism by which

the gate to pain can be closed. It would certainly

explain in physiological terms why psychological

approaches to pain management are successful.

The PAG connects to an area in the medulla

called the nucleus raphe magnus (NRM). This in

turn sends fibres down the spinal cord and they

interact at the dorsal horn. Therefore, higher brain

centres have the infrastructure to open or close

the gate to pain in the substantia gelatinosa.

Substance P is a neurotransmitter that has been

implicated in the transmission of pain, but there

are also several peptides that have been implicated

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Chapter 4 Local anaesthetics and analgesics

in the brain’s analgesic system. The three families

of these peptides are endorphins, dynorphins and

enkephalins. The discovery of these proteins has

been very valuable in our understanding of why

opiate drugs, including morphine, have such a

unique effect on the body.

Types of pain

Nociceptive (tissue) pain

Nociceptive pain results from tissue damage.

Intact pain pathways report this damage via their

neurones, and pain is experienced. Nociceptive

pain can be further subdivided into somatic and

visceral (gut) pain. It can be experienced as sharp,

dull or aching pain. There may be radiation of the

pain, especially visceral pain, but it will not be in

a direct nerve distribution. For example, gall blad-

der pain can radiate to the tip of the left shoul-

der blade. Nociceptive pain generally responds

to NSAIDs and opioids, both of which will be

addressed later in this chapter. Conditions associ-

ated with inflammation, bone pain and joint dis-

ease are particularly responsive to NSAIDs.

Neuropathic (nerve) pain

Neuropathic pain may occur when there is either

damage to or dysfunction of nerves in the periph-

eral or central nervous system. This results in

faulty signals being sent to the brain and expe-

rienced as pain. Neuropathic pain can be either

peripheral (outside the central nervous system)

or central (spinal cord and brain) in origin. Exam-

ples of neuropathic pain include diabetic neuropa-

thy, trigeminal neuralgia, postherpetic zoster pain

(peripheral pains) and thalamic pain syndrome (a

central pain). Neuropathic pain frequently exists

alongside nociceptive pain. Examples include

trauma that damages tissue and nerves, burns (that

burn skin as well as nerve endings) and external

nerve compression. Examples of the latter include

tumours that press on (compress) nerves and the

pain of sciatica, caused by herniated interverte-

bral discs pressing on nerves.

Patients often describe neuropathic pain as a

‘burning sensation’. They may also describe it as

feeling like an electric shock or lightning bolt.

Sometimes, stimuli that usually do not cause

pain, such as light touch, may elicit a painful

response. A light stroke of the cheek that results in

the sudden pain of trigeminal neuralgia is an exam-

ple of this type of pain. Sometimes patients do not

describe the sensation as being ‘painful’ but rather

as feeling unpleasantly strange or ‘tingly’, rather

like an arm feels when it wakes up from ‘going to

sleep’. This is called a dysesthesia. Diabetic neu-

ropathy commonly results in this type of sensation.

Neuropathic pain in the peripheral nervous sys-

tem frequently follows a nerve distribution. This

distribution may follow a particular nerve, as in sci-

atic pain or trigeminal neuralgia, or may represent

the distribution of terminal nerve endings, as in the

‘stocking-glove’ distribution of peripheral neuropa-

thies. Neuropathic pain is relatively resistant to

NSAIDs and opioids, although they may be helpful

in certain cases. The other major classes of medica-

tions useful for neuropathic pain, tricyclic antide-

pressants and gabapentin, will be discussed later.

Acute and chronic pain

Pain can also be classified in terms of how long

a person has experienced it for. A short duration

would be classed as acute pain whereas a longer

duration would be classified as chronic pain.

Acute pain

Acute pain is of recent onset and of limited duration.

Sufferers often describe it as being sharp or stab-

bing in nature, at times like an electric shock. This

is a warning to the body that something is not right

and that damage to cells may be occurring. Exam-

ples of conditions that might lead to acute pain are:

■ bone fracture;

■ after having surgery;

■ following first degree burns;

■ lacerations to the skin;

■ giving birth;

■ dental surgery.

Acute pain can be measured on a scale. It can

be a generally mild pain that soon disappears, or

it might go to the other end of the scale where a

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