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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 eectsRare.
NSAIDsGood for inammatory pain, renal or biliary colic, and bonepain;
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 eects 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 eects, or major comorbidity). Both NSAIDs and COX- 2 inhibitors are associated with increased risk of MI and CVA; use with caution in those atrisk.
• Ibuprofen 400mg/ 6h, max 2.4g/ 24h PO, weaker anti- inammatory
action, but less risk of GI ulceration
• Diclofenac 50mg/ 8h, max 50mg/ 24h PO/ PR (also IM/ IV, seeBNF).
COX- 2 inhibitorsThese 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 (Table2.3).
Side eectsN+V, constipation, drows iness,
others and less constipating for long- termuse. Serotonergic eect.
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 specied
•
Co- dydramol 0mg dihydrocodeine and 500mg paracetamol; two
tablets/ 6hPO.
93PAIN
Table2.3 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 CHAPTER2 Life onthewards
Strong opioidsMorphine 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 eects, 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/ hdoses.
NaloxoneThis given orally antagonizes the constipating eects of opioids,
but is metabolized on ‘rst pass’ through the liver and does not interfere with analgesic eects. Compound preparations of oxycodone/ naloxone (eg Targinact develop painful constipation despite regular laxatives.
Other analgesic options/ adjuncts
Hyoscine butylbromideeg 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;
ContraindicationsRespiratory compromise/ failure, sleep apnoea; Side eects
Drowsiness, confusion, physical dependence (use for short- termonly).
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. Abackground 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. Alocal 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 (Box2.) 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 Inltration 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 driverThese are used mainly for palliative analgesia and symptom con-
trol (Ep. 244).
®
or morphine sulfate solution 0mg/ 2– 4h
O for injections
2
®
dose=half total daily oral morphine requirement
®
) may be of benet for chronic pain relief in those who
®
20mg/ 6h PO/ IM/ IV. This gives good an-
Contraindications Paralytic ileus, prostatism, glau-
Side eects Constipation, dry mouth,
Neuropathic and chronicpain
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 dicult to describe or pinpoint and is often aching, burning, throbbing, or shooting in nature. Chronic conditions can cause signicant pain, eg chronic pancreatitis, arthritis, post- traumatic, DM, trigeminal neuralgia; there is frequently a psychogenic component. Standard analgesia is often ineective and the services of a chronic pain specialist should be sought. Commoner chronic pain therapies include:
Tricyclic antidepressantsGiven at a low dose; Contraindications Recent MI,
arrhythmias; rst- line treatment for neuropathic pain according to NICE guidance.
Side eects Dry mouth, constipation, sedation. This is the
4
• Amitriptyline 0– 75mg/ 24hPO.
Pregabalin Contraindications Hypersensitivity, pregnancy, lactation; Side
Dizziness, tiredness, cerebellar signs. Can be used instead of ami-
eects
triptyline as rst- line treatment for neuropathicpain.
•
Pregabalin 75– 300mg/ 2hPO.
Duloxetine Contraindications Uncontrolled hypertension, pregnancy, seiz-
ures;
Side eectsNausea, dizziness, somnolence, dry mouth. First line for
painful diabetic neuropathy. Avoid abrupt discontinuation.
•
Duloxetine 60– 20mg/ 24hPO.
If rst- line drugs are unsuccessful, they should be stopped and a dierent 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 aect
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/ neuropathicpain.
Steroids and nerve blocksInjections 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 ablationThe ablation of sensory and sympathetic nerves
by surgery or injection; used as a last resort in some forms of chronicpain.
Acupuncture Eective 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. Painteam
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/cg73
95PAIN
96 CHAPTER2 Life onthewards
Nutrition
A patient’s nutritional state has a huge eect 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 Table2.4 for nutritional requirements.
Enteral feeding (via thegut)
Oral Most patients manage to consume sucient quantities of hospital
food to stay healthy. If not, consider simple remedies, eg assisted feeding, favourite foods from home, medications for reux/ 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.
GastrostomyOften 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 theblood)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 sucient enteral feeds (eg short gut syndrome) or when gut rest is required.
There is signicant 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 syndromeThis 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
Table2.4 Nutritional requirements
Name Sources Daily requirement Deciency
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
VitaminA (retinoid)
VitaminB (thiamine)
VitaminB2 (riboavin)
VitaminB (niacin)
VitaminB (pantothenic acid)
VitaminB (pyridoxine)
VitaminB (biotin)
VitaminB (folate)
VitaminB (cobalamin)
VitaminC (ascorbic acid)
Vitamin D Fish, liver, fortied
Vitamin E Vegetables, nuts, fruits,
Dairy, yellow or green leafy vegetables, liver, sh
Bread, cereals .2mg Beriberi
Meat, dairy, bread .3mg Ariboavinosis
Meat, sh, bread 6mg Pellagra
3
Meat, egg, grains, potato,
5
vegetables
Meat, fortied cereals .7mg Anaemia
6
Liver, fruit, meat 30micrograms Dermatitis
7
Bread, leafy vegetables,
9
cereals
Meat, sh, fortied
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 CHAPTER2 Life onthewards
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, aected 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 sucient.
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 reux 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
$ Dened 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 inammatory 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, ciprooxacin, 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 dicult—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 anity 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.
Dened 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 diusion 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 dened as vascular, renal/dialysis, neurosurgery, cardiothoracic surgery,
haematology, oncology, transplant, orthopaedics, and all intensive care units.
99HEALTHCARE-ASSOCIATED INFECTIONS
100 CHAPTER2 Life onthewards
Clostridium dicile
$ 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 fromCDI.
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 specic 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 oer antimotility agents (eg loperamide). Faecal microbiota trans­plantation (FMT) is an eective 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 conrmed cases, for advice on how to prevent transmission.
7
8
K Box 2.2 Ecology, Clostridium dicile, 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 sucient. 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/ng99
8
Start smart then focus:Mwww.gov.uk/government/publications/
antimicrobial-stewardship-start-smart-then-focus
COVID
$ On 3 December 209, 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 signicant 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 inltrates 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 eectiveness 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 signicantly reduces the morbidity and mortality
associated with COVID-9. Messenger RNA (mRNA) vaccines (Pzer/ 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 signicantly reduced viral load and hospitalization or mortality compared with placebo.
102 CHAPTER2 Life onthewards
Aggression and violence
The majority of patients have respect for NHS sta; however, under certain circumstances anyone can become aggressive:
• Pain (Epp. 92–5)
• Reversible confusion or delirium, eg hypoglycaemia (Epp. 382–3)
• Dementia (Epp. 384–5)
• Inadequate communication/ fear/ frustration (Ep. 11)
• Intoxication (medications, alcohol, recreationaldrugs)
• 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 specically about pain and worry. Be calm but rm and do not shout or make threats. If this does not help, oer 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 oering 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.
AbuseAbuse 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 (Box2.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 aorded 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.