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X
- •FoundationProgramme
- •Preface
- •Acknowledgements
- •Contents
- •Symbols andabbreviations
- •3 History and examination
- •4 Prescribing
- •5 Pharmacopoeia
- •6 Resuscitation
- •7 Care at the end of life
- •8 Cardiovascular
- •9 Respiratory
- •10 Gastroenterology
- •11 Endocrinology
- •12 Neurology
- •13 Psychiatry
- •15 Haematology
- •17 Emergency department

Paracetamol g/ 4h, max 4g/ 24h PO/ PR/ IV. Reduce IV dose if
<50kg (5mg/kg/4h, max 60mg/kg/24h);
Contraindications Moderate
liver failure; Side eectsRare.
NSAIDsGood for inammatory pain, renal or biliary colic, and bonepain;
Contraindications(BARS) Bleeding (pre- op, coagulopathy), Asthma, Renal
disease, Stomach (peptic ulcer or gastritis). 0% of asthmatics are NSAIDsensitive, try a low dose if they have never used them before. Avoid use
in the elderly. Increased risk of CVA/ MI;
Side eects Worsen renal func-
tion, GI bleeding (upper and lower— co- prescribe a PPI or high- dose
H
- blocker for those at risk:≥65yr, previous peptic ulcer, use of other
2
medicines with GI side eects, or major comorbidity). Both NSAIDs and
COX- 2 inhibitors are associated with increased risk of MI and CVA; use
with caution in those atrisk.
• Ibuprofen 400mg/ 6h, max 2.4g/ 24h PO, weaker anti- inammatory
action, but less risk of GI ulceration
• Diclofenac 50mg/ 8h, max 50mg/ 24h PO/ PR (also IM/ IV, seeBNF).
COX- 2 inhibitorsThese are similar to NSAIDs and share an increased risk
of MI and CVA, but with less risk of gastroduodenal ulceration.
Weak opioids Dependence and tolerance to opioids do not occur with
short- term use for acute pain. Consider prescribing regular laxatives and
PRN antiemetics, use with caution if head injury, iICP, respiratory depression, alcohol intoxication;
hypotension;
•
Codeine 30– 60mg/ 4h, max 240mg/ 24h PO/ IM, constipating
•
Dihydrocodeine 30– 60mg/ 4h, max 240mg/ 24h PO, constipating
•
Tramadol 50– 00mg/ 4h, max 400– 600mg/ 24h PO/ IM, stronger than
Toxicity dRR, dGCS, pinpoint pupils (Table2.3).
Side eectsN+V, constipation, drows iness,
others and less constipating for long- termuse. Serotonergic eect.
Paracetamol and weak opioid combinations Useful for TTO analgesia; it is
better to prescribe the components separately in hospital:
•
Co- codamol 30mg codeine and 500mg paracetamol; two tablets/ 6h
PO, nurses must give 8/ 500 dose if 30/ 500 not specied
•
Co- dydramol 0mg dihydrocodeine and 500mg paracetamol; two
tablets/ 6hPO.
93PAIN
Table2.3 Opioid conversions
Opioid Potency Equivalent dose to 0mg
Weak opioid (codeine,
dihydrocodeine, tramadol)
Morphine SC/IM/IV 2 5mg
Oxycodone PO
†
A 25microgram/h fentanyl patch is equivalent to 60mg oral morphine.
‡
Oxycodone SC/IV is twice as potent as oxycodone PO.
Table adapted from Faculty of Pain Medicine Mhttps://fpm.ac.uk/
opioids-aware-structured-approach-opioid-prescribing/dose-equivalents-and-changing-opioids
‡
0. 00mg
.5 6.6mg
oral morphine
†

94 CHAPTER2 Life onthewards
Strong opioidsMorphine is used for severe pain. Use regular fast- acting opi-
oids for acute pain with regular laxatives and PRN or regular antiemetics. See
‘Weak opioids’ for cautions, side eects, and toxicity. Use only one method of
administration (ie PO, SC, IM, or IV) to avoid overdose:
Oral eg Sevredol
•
•
SC/ IM Morphine 0mg/ 2– 4h or diamorphine 5mg/ 2– 4h
•
IV titrate to pain; dilute 0mg morphine into 0mL H
(mg/ mL), give 2mg initially and wait 2min for response. Give mg/ 2min
until pain settled observing RR and responsiveness.
Long- acting opioids These are used after major surgery or in chronic
pain. Use standard opioids initially until morphine requirements known
(E p. 244) then prescribe a regular long- acting dose along with PRN
fast- acting opioids to cover breakthrough pain (equivalent to 5% or
one- sixth of daily requirements). Laxatives will be needed.
•
Oral MST
(E p. 244) given every 2h, usually 0– 30mg/ 2h, max 400mg/ 24h
• Topical Fentanyl patch lasts 72h, available in 2– 00micrograms/ hdoses.
NaloxoneThis given orally antagonizes the constipating eects of opioids,
but is metabolized on ‘rst pass’ through the liver and does not interfere
with analgesic eects. Compound preparations of oxycodone/ naloxone
(eg Targinact
develop painful constipation despite regular laxatives.
Other analgesic options/ adjuncts
Hyoscine butylbromideeg Buscopan
algesia in colicky abdo pain;
coma, myasthenia gravis, porphyria;
confusion, urine retention.
Diazepam This acts as a muscle relaxant, eg spasm with back pain;
ContraindicationsRespiratory compromise/ failure, sleep apnoea; Side eects
Drowsiness, confusion, physical dependence (use for short- termonly).
Patient- controlled analgesia (PCA)This is a syringe driver that gives a bolus of IV
opioid (usually morphine, but occasionally tramadol or fentanyl) when the
patient activates a button. Abackground infusion rate, bolus dose, and maximum bolus frequency can be adjusted to prevent overdose/ pain; changes
to the PCA are usually undertaken by the pain team (Box 2.). The patient
must be alert, cooperative, have IV access, and their pain under control before
starting. Check hospital protocols.
Epidurals These are inserted by the anaesthetist in theatre usually prior to sur-
gery. Alocal anaesthetic infusion (± opioid) anaesthetizes the spinal nerves, and
usually produces a sensory level below which the patient has little or no feeling;
if this level rises too high (higher than T4 (nipples)) there is risk of respiratory
failure. The anaesthetist or pain team (Box2.) usually look after epidurals and
their dosing post- op. Complications include local haematoma, abscess (causes
cord compression, E p. 369), or local infection; if there are concerns about an
epidural speak to the anaesthetist covering acute pain immediately.
Nerve blocks Inltration of local anaesthetic for pain relief eg after rib fractures
(paravertebral, serratus plane, or intercostal block) or neck of femur fracture
(fascia iliaca block).
Syringe driverThese are used mainly for palliative analgesia and symptom con-
trol (Ep. 244).
®
or morphine sulfate solution 0mg/ 2– 4h
O for injections
2
®
dose=half total daily oral morphine requirement
®
) may be of benet for chronic pain relief in those who
®
20mg/ 6h PO/ IM/ IV. This gives good an-
Contraindications Paralytic ileus, prostatism, glau-
Side eects Constipation, dry mouth,

Neuropathic and chronicpain
Neuropathic pain is caused by damage to or chronic stimulation of nerve
bres, eg radiculopathy (nerve root pain), peripheral neuropathy, and
phantom limb pain. The pain tends to be dicult to describe or pinpoint and
is often aching, burning, throbbing, or shooting in nature. Chronic conditions
can cause signicant pain, eg chronic pancreatitis, arthritis, post- traumatic, DM,
trigeminal neuralgia; there is frequently a psychogenic component. Standard
analgesia is often ineective and the services of a chronic pain specialist should
be sought. Commoner chronic pain therapies include:
Tricyclic antidepressantsGiven at a low dose; Contraindications Recent MI,
arrhythmias;
rst- line treatment for neuropathic pain according to NICE guidance.
Side eects Dry mouth, constipation, sedation. This is the
4
• Amitriptyline 0– 75mg/ 24hPO.
Pregabalin Contraindications Hypersensitivity, pregnancy, lactation; Side
Dizziness, tiredness, cerebellar signs. Can be used instead of ami-
eects
triptyline as rst- line treatment for neuropathicpain.
•
Pregabalin 75– 300mg/ 2hPO.
Duloxetine Contraindications Uncontrolled hypertension, pregnancy, seiz-
ures;
Side eectsNausea, dizziness, somnolence, dry mouth. First line for
painful diabetic neuropathy. Avoid abrupt discontinuation.
•
Duloxetine 60– 20mg/ 24hPO.
If rst- line drugs are unsuccessful, they should be stopped and a dierent
neuropathic agent started instead. If this is unsuccessful then referral for
a specialist opinion should be considered. The following are examples of
more advanced therapies a pain specialist may prescribe.
TENS Transcutaneous Electrical Nerve Stimulation is believed to aect
the gate mechanism of pain bres in the spine and/ or to stimulate the
production of endorphins. Use at a high frequency for acute pain or slow
frequency for chronic/ neuropathicpain.
Steroids and nerve blocksInjections of steroids combined with local anaes-
thetic into joints or around nerves can reduce pain for long periods. This
needs to be done by a specialist.
Sympathectomy and nerve ablationThe ablation of sensory and sympathetic nerves
by surgery or injection; used as a last resort in some forms of chronicpain.
Acupuncture Eective in some trials and with a greater evidence base than
most complementary therapies.
Counselling and cognitive behavioural therapy (CBT) to develop coping
strategies are widely studied in chronic pain and may be considered by
appropriately skilled specialists. Concern remains that it makes things
worse for some patients.
K Box 2. Painteam
Most hospitals have pain teams, often subdivided into acute and
chronic services. These comprise nurses and a pain specialist (usually an anaesthetist). The acute pain service is sometimes run by the
Outreach Team. In- patients with pain issues can be referred to the
teams for assessment, though ensure all simple measures have been
undertaken to address the patient’s pain rst.
4
NICE guidelines available at Mwww.nice.org.uk/guidance/cg73
95PAIN

96 CHAPTER2 Life onthewards
Nutrition
A patient’s nutritional state has a huge eect on their well- being, mood,
compliance with treatment, and ability to heal. You should consider
alternative nutrition for all patients without a normal oral diet for over
48h. IV uids are only for hydration, they are not nutrition. See Table2.4
for nutritional requirements.
Enteral feeding (via thegut)
Oral Most patients manage to consume sucient quantities of hospital
food to stay healthy. If not, consider simple remedies, eg assisted feeding,
favourite foods from home, medications for reux/ heartburn (E p. 308)
or nausea (E p. 84). If they are still not consuming adequate nutrition
then discuss with the dietician who can advise on supplements.
Nasogastric (NG)(E p. 577 for insertion procedure.) This is a good short-
term measure, however placing the tube may be uncomfortable and some
people nd the sensation of the tube uncomfortable once it is in. Liquid
foods and most oral medicines (except slow- release and enteric- coated
preparations) can be given via NG tube; advice regarding medications via
this route may be required from a pharmacist. Tubes can also be endoscopically placed naso- jejunally if required, eg gastric outlet obstruction.
GastrostomyOften called ‘PEGs’ (percutaneous endoscopic gastrostomies),
these are a good long- term method of feeding for patients who cannot
feed orally. They are typically sited endoscopically, though surgical and
radiological approaches are possible (a radiologically inserted gastrostomy
is referred to as a RIG). It is also possible to place a jejunostomy if required.
Parenteral feeding (via theblood)Parenteral nutrition (PN) or
total parenteral nutrition (TPN) requires central access because extravasation of the feed causes severe skin irritation. Central access can be via
a long- line (eg peripherally inserted central catheter) or central line (eg
Hickman). It is used when the patient cannot tolerate sucient enteral
feeds (eg short gut syndrome) or when gut rest is required.
There is signicant risk associated with PN use including line insertion, line
infection, embolism/ thrombosis, and electrolyte abnormalities. It is essential to monitor blood electrolytes regularly including Ca
zinc, and trace elements, particularly in those starting PN after a period
of malnutrition (see next paragraph).
Refeeding syndromeThis refers to the potentially fatal electrolyte
disturbances that occur on refeeding malnourished patients. Classically,
there is dPO
–
3
4
, dK+, and dMg2+ which can lead to arrhythmia and seiz-
ures. Those at risk include patients with low BMI, recent unintentional
weight loss, starvation for >5d, and a history of alcohol excess.
Treatment Feeding should be introduced slowly under the supervision of the
dietitians; often this is introduced at 0kcal/kg/d and gradually increased.
Measure PO
–
3
4
, K+, and Mg
2+
before initiation and during the rst 3–5d,
correcting low levels with oral or parenteral replacement promptly. Highrisk patients should also receive oral thiamine (eg 00mg/BD), vitamin B
co-strong (tab/TDS), and multivitamin (eg Forceval
5
NICE guidelines available at Mwww.nice.org.uk/guidance/cg32
2+
, PO3 4 –, Mg2+,
®
tab/OD) for 0d.
5

Nutritional requirements
Table2.4 Nutritional requirements
Name Sources Daily requirement Deciency
Carbohydrate Almost all foods 300g Malnutrition
Pro tein Meat, dairy, vegetables, grain 50 g Kwas hior kor
Fat Nuts, meat, dairy, oily
foods
Calcium Dairy, leafy vegetables g Osteoporosis
Iodi ne Fish, seafood, enriched salt 50microgra ms Hypothyroid
Iron Meat, vegetables, grains 5mg Anaemia
Mag nesium Dairy, leafy vegetables, meat 420mg Cra mps
Potassium Fruits, vegetables 3.5g Hypokalaemia
Selenium Meat, sh, vegetables 55micrograms Keshan disease
Sodium Processed foods, salt 2.4g Hyponatraemia
Zinc Cereals, meat mg Hair/ skin
VitaminA
(retinoid)
VitaminB
(thiamine)
VitaminB2
(riboavin)
VitaminB
(niacin)
VitaminB
(pantothenic
acid)
VitaminB
(pyridoxine)
VitaminB
(biotin)
VitaminB
(folate)
VitaminB
(cobalamin)
VitaminC
(ascorbic acid)
Vitamin D Fish, liver, fortied
Vitamin E Vegetables, nuts, fruits,
Dairy, yellow or green
leafy vegetables, liver, sh
Bread, cereals .2mg Beriberi
Meat, dairy, bread .3mg Ariboavinosis
Meat, sh, bread 6mg Pellagra
3
Meat, egg, grains, potato,
5
vegetables
Meat, fortied cereals .7mg Anaemia
6
Liver, fruit, meat 30micrograms Dermatitis
7
Bread, leafy vegetables,
9
cereals
Meat, sh, fortied
2
cereals
Citrus fruits, tomato,
green vegetables
cereals
cereals
Vitamin K Green vegetables, cereals 20micrograms
56g Malnutrition
problems
900micrograms Night
blindness
5mg Neurological
problems,
paraesthesia
400micrograms Anaemia
2.4micrograms Anaemia
200mg Scurvy
5– 5micrograms Rickets/
osteomalacia
5mg None
iPT
97NUTRITIONAL REQUIREMENTS

98 CHAPTER2 Life onthewards
Healthcare-associated infections
Controlling the spread of pathogens from an infectious source is essential in healthcare settings. Standard precautions include hand hygiene
(using soap and water if hands are visibly soiled), environmental cleaning,
safe disposal of sharps to avoid needle-stick injuries, waste disposal, and
respiratory hygiene (eg covering mouth and nose when coughing and
sneezing). Further precautions depend on the mode of transmission:
Contact Patients should be isolated in a side room with dedicated
equipment. PPE (gloves, gown) should be donned upon room entry for
all interactions involving the patient or their environment and should
be disposed of before exiting the room. The environment should be
fully disinfected prior to use by another patient.
Droplet In addition to contact precautions, PPE should include a sur-
gical mask and the patient should wear a mask while being transported.
Airborne In addition to droplet precautions, the patient should be
isolated in a negative pressure isolation room and masks should be ttested (eg FFP3 mask).
Norovirus
$ Non-enveloped, single-stranded RNA virus. In the UK, outbreaks are
common in winter (‘winter vomiting disease’).
Transmission Via the faeco– oral route, either through contact with in-
fected individuals or contaminated surfaces or food. A small inoculum
(<00 particles) is required for infection.
Clinical features After a 24–48h incubation period, aected individuals de-
velop diarrhoea and vomiting lasting for 2–3d.
Detection Usually by reverse transcription polymerase chain reaction
(RT-PCR) of stool sample, though clinical diagnosis in the context of an
outbreak is usually sucient.
Treatment Supportive. IV uid replacement for severe dehydration.
Catheter-associated infections
Urinary tract infections (UTIs) are one of the largest groups of hospitalacquired infections. Risk factors for catheter-associated UTI include advanced age, diabetes, immunosuppression, and the duration of catheter.
Sterile equipment and aseptic technique should be used for catheter insertion. Antibiotic prophylaxis may be indicated in some patients, such as
those with recent culture-positive UTI or undergoing joint replacement—
check local protocols. Catheter bags should be emptied frequently to prevent reux and catheters should be removed as soon as possible.
Line infections
Infection may arise from contamination with skin ora or as part of systemic infection. Common pathogens include Staphylococcus aureus,
coagulase-negative staphylococci and Streptococcus. Infection risk is greatest
with central lines, but the overall morbidity is highest for peripheral cannulas as they are so widely used. Almost all peripheral cannula-associated
infections are preceded by visible phlebitis or cellulitis, which should be a
trigger for cannula removal.
Prevention Strict aseptic non-touch technique should be followed when
inserting or using an IV vascular device.

Hospital-acquired pneumonia
$ Dened as pneumonia occurring >48h after admission.
Cause Gram-negative enterobacteria, S. aureus, Pseudomonas, Klebsiella,
Bacteroides. Bacteria may be introduced into the lungs by aspiration,
haematogenous spread from IV lines, from leakage of secretions around
an endotracheal tube cu, or inhalation.
Transmission Via the contaminated hands of healthcare workers, via med-
ical devices or the environment.
Risk factors Poor infection control practices, aspiration, decreased GCS,
intubation and ventilation, major surgery, long hospital stay.
Detection Consider CXR in any hospitalized patient with fever, unexplained
rise in inammatory markers, new oxygen requirement, or dyspnoea.
Sputum culture with sensitivity testing.
Management Local antibiotic choices vary based on local sensitivity data,
check hospital policy. Initial treatment usually involves broad-spectrum
antibiotics such as anti-pseudomonal penicillins (eg piperacillin/tazobactam)
or a 3rd-generation cephalosporin.
Carbapenemase-producing Enterobacterales (CPE)
$ CPE are increasingly associated with hospital- and community-acquired
infections. CPE are resistant to carbapenems alongside most other antibiotic classes including penicillins, ciprooxacin, and gentamicin.
Transmission By direct contact or via contaminated objects.
Detection Via rectal swab or stool culture if rectal swab is not available.
Management Treating incidental colonization is not required but isolate with
contact precautions; treating infection is dicult—discuss with microbiology.
MRSA
$ MRSA stands for meticillin-resistant Staphylococcus aureus. First detected
in 96, resistance to β-lactam antibiotics is conferred by the mecA gene
which produces an alternative cell wall protein PBP2a with a low anity for
β-lactams. The last decade has seen a fall in MRSA rates in the UK as a result
of infection control practices and national mandatory surveillance.
Transmission By direct skin-to-skin contact or via contaminated objects.
Dened as either healthcare-acquired (occurring >48h after admission) or
community-acquired.
Clinical features Often asymptomatic colonization of the skin and soft tis-
sues. Symptomatic infections are similar to those caused by S. aureus but
patients have a higher mortality and longer in-patient stays.
Detection Swab nostrils, perineum, or other site where appropriate. Screening
via detection of the mecA gene or culture on chromogenic agar, followed by
full culture and resistance testing (eg cefoxitin disc diusion test).
Screening Current UK government guidelines recommend mandatory
screening of two patient groups: patients admitted to high-risk units
6
and
those with previous MRSA colonization or infection.
Treatment In asymptomatic colonization, eradication can be achieved by a com-
bination of nasal mupirocin and antiseptic body washes. Symptomatic infections can be treated by glycopeptides (vancomycin or teicoplanin), daptomycin,
linezolid, and quinupristin with dalfopristin. Discuss with microbiology.
6
High-risk units are dened as vascular, renal/dialysis, neurosurgery, cardiothoracic surgery,
haematology, oncology, transplant, orthopaedics, and all intensive care units.
99HEALTHCARE-ASSOCIATED INFECTIONS

100 CHAPTER2 Life onthewards
Clostridium dicile
$ A Gram- positive spore- forming anaerobic bacillus which can asymptomatically colonize the gut (Box 2.2). Exposure to antibiotics alters the balance
of gut ora, promoting C. di overgrowth, production of toxins that damage
colonic mucosa, and subsequent symptomatic C. di infection(CDI) (Box 2.2).
Transmission Via the faeco– oral route, after direct or indirect contact
between patients, or ingestion of spores in the environment.
Clinical features Watery diarrhoea, abdominal pain, fever, and leucocytosis.
Severe disease causes pseudomembranous colitis and toxic megacolon.
Elderly and frail patients are at especially high risk of dehydration, recurrent disease, and mortality fromCDI.
Detection Currently this involves a 2- stage process using stool samples,
with a rapid screening test for C.di glutamate dehydrogenase (or PCR
for the C.di toxin gene), followed by a more specic immunoassay for
the C.di toxin. Consider urgent AXR to rule out toxic megacolon.
Treatment First-line therapy for mild, moderate, or severe infection is
vancomycin 25mg/ 6h PO for 0d. Fidaxomicin 200mg/2h PO for
0d is second line. Pay attention to uid and electrolyte balance and
review any exacerbating medications (eg antibiotics, PPIs, laxatives). Do
not oer antimotility agents (eg loperamide). Faecal microbiota transplantation (FMT) is an eective treatment for refractory or recurrent
cases (>2 previous episodes). Life-threatening cases may be treated with
vancomycin 500mg/6h PO plus metronidazole 500mg/8h IV for 0d.
Bezlotoxumab, a monoclonal antibody against C. di toxin B, is not currently recommended by NICE.
Infection control
Barrier nursing, good hand hygiene, and cleaning of equipment is key to preventing transmission to other patients (the spores are
resistant to alcohol hand gels so handwashing with soap is essential).
Local infection prevention teams should be made aware of suspected
and conrmed cases, for advice on how to prevent transmission.
7
8
K Box 2.2 Ecology, Clostridium dicile, and antibiotics
Intestinal carriage of C. di does not equate with disease— what
matters is when it outgrows other colonic commensal bacteria.
Hence just controlling transmission is not entirely sucient. Instead,
we need to avoid disturbing the healthy colonic ora through indiscriminate use of broad- spectrum antibiotics. As part of this approach, most hospitals limit the use of cephalosporins, quinolones,
and clindamycin. The national toolkit on antibiotic stewardship
8
aids
clinicians in reducing CDI rates as well as antimicrobial resistance.
Always prescribe using local antibiotic guidelines, and regularly review whether prescriptions are needed.
7
NICE clinical guidelines available at:Mwww.nice.org.uk/guidance/ng99
8
Start smart then focus:Mwww.gov.uk/government/publications/
antimicrobial-stewardship-start-smart-then-focus

COVID
$ On 3 December 209, the WHO was informed of cases of pneumonia of
unknown microbiological aetiology in Wuhan City, China. The novel agent was
a betacoronavirus, severe acute respiratory syndrome coronavirus 2 (SARSCoV-2). The infectious disease was named COVID-9 after the year of its
discovery, and quickly spread across the globe causing millions of deaths worldwide. The majority of patients in the initial stages of the outbreak reported a link
to the Huanan South China Seafood Market, a live animal market. In the UK,
a signicant proportion of cases are associated with nosocomial transmission.
Cause SARS-CoV-2, a novel enveloped RNA virus. Several variants have
emerged over time, named using the Greek alphabet.
Transmission Via droplets or aerosols, commonly in areas with poor ven-
tilation. Aerosol-generating procedures include intubation and ventilation,
CPR, non-invasive ventilation, and surgical procedures.
Clinical features Generally presents as respiratory infection on a spectrum
from mild common cold-like illness to severe pneumonitis requiring invasive ventilation. Fever, cough, and loss of smell/taste are common. CXR
typically shows bilateral patchy inltrates and lymphopenia is common;
consider superadded bacterial infection if neutrophilia is present. Severe
disease may be complicated by venous or arterial thromboembolism,
cerebral haemorrhage, and multiorgan failure. Prolonged symptoms may
be experienced by some individuals—termed ‘long COVID’.
Detection Via RT-PCR on nasal or pharyngeal swab. Rapid antigen tests
detecting SARS-CoV-2 viral proteins in upper respiratory tract secretions are less sensitive than RT-PCR, but are a widely available means of
detecting infectious individuals with a high viral load who may be otherwise
asymptomatic.
Treatment Guidelines are changing rapidly as new drugs are developed
and evidence for the eectiveness of treatment emerges (eg RECOVERY
9
trial
). Management depends on the severity of disease and the functional
status of the patient, which can be assessed using scoring systems such as
the Clinical Frailty Scale. For immunocompromised or comorbid patients
at risk of developing severe disease, weak evidence suggests that antiviral
agents (molnupiravir
0
) or monoclonal antibody treatment (sotrovimab)
reduce the risk of hospital admission if taken early after testing positive.
For hospitalized patients requiring supplemental oxygen, dexamethasone
(6mg/24h PO/IV) for 0d has been shown to reduce 28d mortality. In
severe disease, a trial of CPAP may be appropriate and strong evidence
exists for the use of IL-6 blockers (eg tocilizumab).
Prevention Vaccination signicantly reduces the morbidity and mortality
associated with COVID-9. Messenger RNA (mRNA) vaccines (Pzer/
BioNTech, Moderna) are approved for use in the UK.
101HEALTHCARE-ASSOCIATED INFECTIONS
9
The RECOVERY trial recruited participants >2yr who were hospitalized with COVID-9 from
27 sites in the UK between 8 September 2020 and 22 May 202.
0-
The MOVe-OUT trial recruited 433 patients in 20 countries within 5d of symptom onset and
randomized to either molnupiravir or placebo. Molnupiravir was associated with signicantly
reduced viral load and hospitalization or mortality compared with placebo.

102 CHAPTER2 Life onthewards
Aggression and violence
The majority of patients have respect for NHS sta; however, under
certain circumstances anyone can become aggressive:
• Pain (Epp. 92–5)
• Reversible confusion or delirium, eg hypoglycaemia (Epp. 382–3)
• Dementia (Epp. 384–5)
• Inadequate communication/ fear/ frustration (Ep. 11)
• Intoxication (medications, alcohol, recreationaldrugs)
• Mental illness or personality disorder (E pp. 386–89).
The aggressive patient Ask a nurse to accompany you when as-
sessing aggressive patients. Position yourselves between the exit and the
patient and ensure that other sta know where you are. The majority of
patients can be calmed simply by talking; try to elicit why they are angry
and ask specically about pain and worry. Be calm but rm and do not
shout or make threats. If this does not help, oer an oral sedative or give
emergency IV sedation (E p. 378) or call hospital security.
The aggressive relative Relatives may be aggressive through fear,
frustration, and/ or intoxication. They usually respond to talking, though
make sure you obtain consent from the patient before discussing their
medical details. Consider oering to arrange a meeting with a senior
doctor. If the relative continues to be aggressive, remember that your duty
of care to patients does not extend to their relatives; you do not have to
tell them anything or listen to threats/ abuse. In extreme cases you can ask
security or police to remove the relative from the hospital.
Violence Assault (the attempt or threat of causing harm) and battery
(physical contact without consent) by a patient or relative is a criminal offence. If you witness an assault or are assaulted yourself, inform your seniors
and ll in an incident form including the name and contact details of any
witnesses. If no action is taken on your behalf, inform the police yourself.
AbuseAbuse is a violation of an individual’s human and civil rights and may con-
sist of a single act or repeated actions. It may be physical, sexual, nancial, psychological, or through neglect. Patients of any age can be abused. Do not be afraid of
asking patients how they sustained injuries or asking directly if someone caused
them. Inform a senior if you suspect a patient has been abused (Box2.3).
K Box 2.3 Safeguarding and protection
As a doctor you will often meet your patients at their most vulnerable
moments. In most instances, the forces of nature will have conspired
to weaken the individual to bring them to this point. But in sad and rare
cases, vulnerable individuals are not aorded the protection they need,
and a presentation to acute healthcare services may be a manifestation
of abuse. Two groups are particularly at risk:vulnerable adults (those in
need of community services because of mental or other illness, disability,
or age) and children. While government policy on protecting these groups
continues to evolve, and new statutory regulations are likely to be introduced, your local healthcare organization should have clear policies on
child protection and adult safeguarding. In all instances, your rst and most
important action if you believe a patient may be subject to any form of
abuse is to bring your concerns to the attention of your consultant.
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