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Infectious diseases
cell + proteases
Table37.7 Malignancies seen with increased frequency
and associated viruses
Tumour Associated virus
Kaposi sarcoma Human herpesvirus 8
Cerebral lymphoma Epstein–Barr virus
Non-Hodgkin lymphoma Epstein–Barr virus
Hodgkin disease Not determined
Cervical carcinoma Human papillomavirus
Anal carcinoma Human papillomavirus
particularly highly active antiretroviral therapy (HAART),
which slows disease progression.
HAART involves a combination of agents from at least
two types of antiretroviral medication:
• nucleoside analogue reverse transcriptase inhibitors
(e.g. zidovudine, lamivudine and didanosine)
• nonnucleoside analogue reverse transcriptase inhibitors
(e.g. efavirenz and nevirapine)
• protease inhibitors (e.g. ritonavir, indinavir and
saquinavir)
Newer drugs include integrase inhibitors (e.g. raltegravir),
fusion inhibitors and CCR5 antagonists (e.g. maraviroc)
(Fig.37.1).
In the United Kingdom treatment is recommended as
soon as HIV diagnosis has been made or in the presence
of AIDS-defining infection or major infection if the CD4
count is less than 200 cells/mL. It aims to deliver a longterm plasma HIV RNA concentration count of less than 50
copies per millilitre.
HIV prognosis is strongly related to and worse with a higher
viral load and lower CD4 count, as these indicate a more rapid
progression from early to late stages of infection. Viral load and
CD4 count are also used to monitor the response to treatment.
As HIV treatment has improved, the incidence of
HIV-associated infection (Table37.8) and malignancy has
changed and in many cases diminished. This means that
even though long-term prognosis in people who respond
well to HAART (high CD4+ counts and unrecordable viral
load) is not known, many are asymptomatic and living normal lives more than 15years after diagnosis.
COMMUNICATION
Do not be afraid to perform an HIV test. It is
important to discuss your intention with the patient.
Remember to remain open and explain well steps
of your management. Remain nonjudgemental
and reassure the patient of the importance of
confidentiality. Allow the patient to be involved in
decision making regarding treatment. Stress the
importance of the current success with regard to
disease outcomes following treatment.
5 Assembly
of more
HIV
Viral
protein
Proteases
Viral
mRNA
4 Protease inhibitors
—inhibit proteins
required in assembly
of new viral particles,
e.g. saquinavir,
ritonavir
Two
copies
of per
and integrases
CCR5 antagonists
e.g. maraviroc
1 Fusion inhibitors
—block entry of virus
e.g. enfurvitide
Coreceptors
CCR5 or
CXCR4
into cell,
HIV
1 Fusion of
HIV with
host cell
2 Production of
RNA
Reverse
transcriptase
2 Reverse transcriptase
inhibitors
—NRTIs, e.g. AZT/ddI
—NNRTIs, e.g. efavirenz
DNA from
viral RNA
DNA
3 Integration
Integrases
of
DNA into
host
DNA
4 Production
of components
of new
HIV
Provirus
3 Integrase
inhibitors
e.g. raltegravir
Fig.37.1 Site of action of HIV drugs. AZT, Zidovudine (also known as ‘azidothymidine’); ddI, didanosine (also known as
‘2′,3′-dideoxyinosine’); mRNA, messenger RNA; NNRTI, nonnucleoside reverse transcriptase inhibitor; NRTI, nucleoside
reverse transcriptase inhibitor.
378
Table37.8 Treatment and prophylaxis of opportunistic infections
Infection Treatment
Pneumocystis
jirovecii
Toxoplasmosis Sulfadiazine plus
Cytomegalovirus Ganciclovir or
Herpes simplex Aciclovir Valaciclovir or
Herpes zoster Aciclovir Valaciclovir or
Cryptococcal
meningitis
Mycobacterium
avium complex
Candida Fluconazole Ketoconazole or
Orally or intravenously
administered
cotrimoxazole
Steroids may be
beneficial
pyrimethamine +
folate
foscarnet
Amphotericin B with
or without flucytosine,
or fluconazole
Rifampicin plus
ethambutol plus
clarithromycin
Treatment
alternatives
Intravenously
administered
pentamidine, or
clindamycin plus
primaquine, or
dapsone plus
trimethoprim
Clindamycin replacing
sulfadiazine
Secondary prevention Ganciclovir or
foscarnet
foscarnet or
famciclovir
Secondary prevention Fluconazole
Rifabutin replacing
rifampicin
itraconazole
Malaria
Indication for
prophylaxis
Secondary prevention
or CD4+ count
<200/μL
Secondary prevention
or CD4+ <200 cells/μL
positive serology
Secondary prevention Aciclovir
Secondary prevention Azithromycin or
Secondary prevention Fluconazole
Prophylactic drug
regimes
Orally administered
cotrimoxazole, or
nebulized pentamidine,
or dapsone plus
pyrimethamine
Pyrimethamine
plus sulfadiazine,
or clindamycin, or
cotrimoxazole, or
dapsone
foscarnet
clarithromycin
3737
Prevention
No ‘cure’ for HIV infection means preventative measures
must remain the highest priority for healthcare professionals. Such measures include education, provision of
clean needles for intravenous drug abusers, use of condoms, screening of blood products and organs donated for
transplantation, and avoidance of breastfeeding in HIVpositive mothers. Research continues into new treatments
and the possibility of a vaccine, and the development of
postexposure prophylaxis has reduced transmission rates
and provides hope for future disease control.
ETHICS
It is common practice to gain consent from the
patient should a healthcare professional sustain a
needle stick injury. Problems arise when a patient
does not have the capacity to consent. The British
Medical Association has established a set of
ethical guidelines medical professionals can follow:
• If a patient is expected to regain capacity before
testing is needed, testing should be withheld
until consent can be obtained.
determine whether legal arrangements have
been set for the patient regarding the matter
(e.g. advanced directive).
• If a patient is not expected to regain capacity
before testing is required, a responsible clinician
can make a decision regarding testing based on
the patient’s best interest.
MALARIA
Epidemiology and aetiology
Worldwide, malaria affects more than 200 million people
and caused more than 400,000 deaths in 2015. It is endemic
in developing countries, with the heaviest toll in Africa. It
can easily be imported by people who have visited or come
379
Infectious diseases
Sporogeny
Gametocytes develop into gametes,
zygotes, ookinetes and oocysts in the
mosquito gut; infective sporozoites
then migrate to the salivary glands and
enter the human circulation when the
mosquito feeds
Table37.9 Plasmodium species causing malaria
Organism Clinical features
Plasmodium
falciparum
Plasmodium
vivax
Plasmodium
ovale
Plasmodium
malaria
Most common worldwide and
responsible for most deaths. Incubation
period is 7–14days, with most travellers
presenting within 8weeks. Classic
features of paroxysmal episodes every
36–48 h are rare or irregular
Incubation period is 12–17days.
Causes benign malaria with tertian
features of symptoms presenting every
3days. Relapse is due to persistent
dormant parasite in the liver
Incubation period is 15–18days.
Presents with relapse similarly to
infection with P. vivax
Incubation period is long at 12–40days.
Can present with quartan malaria (also
known as ‘quartan fever’) every 4days,
which is rare however. Can present late,
1year after initial infection. Dormant
parasites reside in the blood
from endemic areas, and in the United Kingdom, approximately 1500 cases are notified each year.
The disease is caused by protozoal infection with one of
the species of the genus Plasmodium (P. vivax, P. ovale, P.
malariae or P. falciparum) (Table37.9).
Pathology
Malaria is a life-threatening illness that spreads through
a bite of a female Anopheles mosquito. A infective, motile
sporozoite travels through the bloodstream to reach the
liver. There it enters a hepatocyte, where it asexually reproduces (schizogony), leading to the production of millions
of merozoites. These invade new red blood cells (RBCs),
in which they asexually multiply to produce 8–24 infective
merozoites. At this point, RBCs rupture, and the whole cycle
begins again (Fig.37.2). A burst of cells causes the release of
malaria parasites, malaria antigen, cytokines (especially tumour necrosis factor) and other RBC constituents into the
bloodstream, causing the typical clinical picture of periodic
fevers. Depending on the Plasmodium species the timing of
the clinical manifestations differs (see Table37.9). P. vivax,
P. ovale and P. malariae invade up to 2% of the circulating
RBCs. P. falciparum may affect more than 10% of RBCs,
producing a potentially severe illness.
Clinical features
Malaria presentation is determined by parasitaemia levels and corresponds to the parasite life cycle. Symptoms
may occur from 6days after initial infection up to several months later. It is characterized by periodic high
temperature, sweating and rigours, which coincide with
the release of merozoites from erythrocytes. Nausea and
Fig.37.2 The malaria transmission cycle.
Exo-erythrocyctic (hepatic)
2
1
Sporozoites infect liver cells and these
mature into merozoites, which pass
into the bloodstream
3
Erythrocyctic
Merozoites infect red blood cells
and become trophozoites; these
release more merozoites; some
develop into male or female
gametocytes, which infect the
mosquito when it takes up blood
380
Diarrhoeal disease
3737
vomiting, abdominal pain, diarrhoea, headache, cough
and arthralgia/myalgia may also be present. Splenomegaly
is commonly found, but mild jaundice and hepatomegaly
may also be present. Complications are almost always
associated with P. falciparum, and are summarized in
Table37.9.
The diagnosis is confirmed by:
• Thin and thick blood films (gold standard tests). If
there is clinical suspicion of malaria but the blood film
is negative, a further two samples over the subsequent
48 hours are necessary to rule out the infection.
• Rapid diagnostic tests that detect parasite antigens.
These are dipstick based and can be used by staff who
have not been trained in microscopy. They are more
expensive, however, but together with microscopy
studies are recommended as diagnostic tests for
malaria by WHO.
• Polymerase chain reaction. This is more sensitive
than microscopy, but takes much longer and is most
useful when you are considering epidemiological
testing.
Other investigations frequently used include:
• Full blood count: this may show anaemia, leucocytosis
and thrombocytopenia.
• Liver functions tests: enzyme levels are often
deranged.
• Urea and electrolyte measurements: these show raised
creatinine level and hyponatraemia.
Hypoglycaemia may be seen.
Treatment and prognosis
The treatment of malaria is under constant review as resistant strains develop. It is dependent on the severity of the
disease and strain of Plasmodium.
Non-falciparum malaria is treated with:
• chloroquine (first line)
• quinine
• primaquine (used for prevention and resistant disease)
Uncomplicated falciparum malaria is treated with:
• orally administered quinine plus doxycycline/
clindamycin
• atovaquone–proguanil (Malarone)
• artemether–lumefantrine (Riamet)
Complicated falciparum malaria is treated with:
• intravenously administered quinine dihydrochloride
followed by orally administered quinine plus
doxycycline/clindamycin
• artesunate regimen plus doxycycline/clindamycin
If left untreated malaria can be deadly (Table37.10). Of par-
ticular concern is cerebral malaria, with a mortality rate of
20%. Improvement of management and prevention, however, has led to a decrease in overall worldwide mortality
rates by 60% in the last decade.
Table37.10 Complications of infection by Plasmodium
falciparum
Cerebral malaria (hyperpyrexia, coma, death)
Hypoglycaemia
Acute respiratory distress syndrome
Seizures
Severe intravascular haemolysis with haemoglobinuria
(blackwater fever)
Acute renal failure
Hepatic necrosis
Jaundice
Haemolytic anaemia
Lactic acidosis
Coagulopathy (including disseminated intravascular
coagulation)
COMMUNICATION
Travellers need careful instruction about the need
for malaria prophylaxis, both medication and
precautions against mosquito bites.
It is important to stress preventative measures
are effective but are not a guarantee against the
infection.
Prevention
Use of chemoprophylaxis together with insecticide-treated
nets results in a prevention rate of 90%. Medications used
include chloroquine, proguanil–atovaquone, mefloquine
and doxycycline. Other protective behaviours to avoid mosquito bites, including wearing covered clothes and using insect repellent, are also important.
DIARRHOEAL DISEASE
Diarrhoea is one of the most common reasons for which
people seek medical attention, and diarrhoeal disease is
the second leading cause of death in children younger than
5years of age according to WHO. It can last for days and can
deplete essential stores of water and electrolytes.
Diarrhoea is defined as the passage of three or more
loose stools in a day, and is usually caused by infective bacteria, viruses or parasites Tables 37.11. Most commonly it
spreads through the enteral route, and this is through contaminated water or poor hygiene.
Three distinct forms of diarrhoea can be characterized:
• acute watery diarrhoea; caused by infection, drugs
and other factors, including stress, allergies and other
medical conditions;
381
Infectious diseases
Table37.11 Causes of diarrhoea
Organism
type Causes of diarrhoea
Viruses Norovirus (most common
cause of diarrhoea worldwide)
Rotavirus
Sapovirus
Bacteria Salmonella
Campylobacter jejuni
Shigella
Escherichia coli (most
common in the elderly)
Parasites Cryptosporidium parvum
Giardia intestinalis
Entamoeba histolytica
Cyclospora cayetanensis
Table37.12 Causes of bloody diarrhoea
Organism type Causes of bloody diarrhoea
Bacteria Campylobacter jejuni
Salmonella
Escherichia coli O157:H7
Clostridium difficile
Shigella
Vibrio parahaemolyticus
Yersinia
Aeromonas
Viruses Cytomegalovirus
Parasites Entamoeba histolytica
Schistosomiasis
Length of
symptoms
2–3days
3–5days
Weeks to
months if
untreated
• acute bloody diarrhoea; caused by infective organisms
(Table37.12);
• persistent diarrhoea (>14days); associated with
chronic bowel conditions (inflammatory bowel
disease, irritable bowel syndrome, diverticular disease
and malignancy), infection, coeliac disease and
malabsorption, constipation and drugs.
Most dangers of diarrhoeal disease come from dehydration.
Management involves initial assessment of the severity,
the presence of red flag symptoms and determination of
a cause. Assessment of complications such as dehydration
will determine treatment but focuses on replacement of
water and electrolytes. Investigations are not always necessary but may include stool sample for culture and sensitivity
testing and blood tests.
DRUG-RESISTANT BACTERIA
The last decade has seen an increase in the emergence of
drug-resistant strains of bacteria, commonly ascribed to
overuse of low-dose antibiotics, which exert an environmental pressure on the pathogens. Drug resistance may be
acquired via mutation or bacterial plasmid transfer.
Drug-resistant bacteria are important in terms of mortality, morbidity and increased cost and as a healthcare
professional the single biggest contribution to be made
to limiting spread is adherence to local infection control
protocols.
Methicillin-resistant
Staphylococcus aureus
Infection with methicillin-resistant Staphylococcus aureus
(MRSA) results in the same range of presentations as other
S. aureus infections, including skin, respiratory and urinary
tract infections, but is highly resistant to antibiotic therapy.
It is often acquired during exposure in healthcare facilities but most of the time does not cause harmful infection.
MRSA is resistant to most β-lactam antibiotics, but is often
sensitive to tetracyclines, glycopeptides (vancomycin and
teicoplanin) rifampicin and sodium fusidate.
In hospital, patients are routinely screened (nose/axilla/
groin) for MRSA. Those who test positive have eradication
therapy and barrier nursing if needed and are managed with
special precautions.
Other resistant bacteria
Vancomycin-resistant enterococci may have emerged because of the increased use of vancomycin for treatment of
MRSA and Clostridium difficile infections. Enterococci are
common gut flora but in at-risk patients may cause urinary
tract infection, wound infections and bacteraemia.
Carbapenem-resistant Enterobacteriaceae (CRE) infections are currently on the rise, and CRE are resistant to
nearly all available antibiotics. It is estimated almost 50%
of patients with CRE-positive blood culture die of the
infection.
Resistant gram-negative bacteria such as Pseudomonas
are a common problem in chronic suppurative respiratory conditions, such as bronchiectasis and cystic fibrosis,
as well as in intensive care units, where they may cause
ventilator-associated pneumonia.
CLINICAL NOTES
Red flag symptoms include blood in stool, recent
hospital treatment or antibiotic administration,
persistent vomiting or high-volume diarrhoea,
recent weight loss and nocturnal symptoms.
382
Drug-resistant bacteria
Chapter Summary
• Infectious diseases including HIV-related disease and malaria are currently a growing
problem in both the developed world and the developing world. The World Health
Organization provides general guidelines to master disease prevention and improve
patient survival. Research aims to improve management and develop a treatment.
• Unfortunately, there is no current cure for HIV infection but hopes have been raised with
the use of antiretroviral treatment, which reduces HIV-associated mortality and morbidity.
This is drawn from great experience gained from a successful fight with currently
preventable and treatable infectious diseases such as malaria.
• Because of overuse of antibiotics and a high mutation rate, however, new treatmentresistant pathogens arise quickly. It is important to continue to take caution when you are
considering infectious disease and ensure all appropriate precautionary measures are
used.
3737
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Drug overdose and abuse
38
GENERAL OVERVIEW
Drug overdose results in a significant proportion of all acute
hospital admissions and has an overall incidence of around
2 per 1000 population. Around 25% of suicides are due to
deliberate drug overdose. Admission following the use of
illicit drugs is also frequently seen – common substances are
given in Tables 38.1 and 38.2.
Overdose may be:
• accidental: particularly in children or patients with
impaired memory or cognition;
• deliberate: in suicide, attempted suicide or deliberate
self-harm, homicide or abuse of vulnerable adults or
children;
• iatrogenic: for example drug interactions, reduced
metabolism/excretion (renal failure, liver failure) or
medical error.
COMMON PRESENTATION, INVESTIGATIONS AND MANAGEMENT
History
In many patients, drug overdose results in a mild illness
requiring little intervention. Some patients take sufficient
medication or mixtures of drugs to cause a life-threatening
situation which requires admission to intensive care. Around
80% of patients are conscious and able to provide a history
when they present. In all patients, particularly the unconscious, further history from family, friends, the patient’s general practitioner and the ambulance staff is likely to be very
helpful and should be actively sought. Always consider the
possibility of an overdose in any unconscious patient. Where
possible, try to establish what drugs were taken and when.
It is very common for the patient to have taken more than
one drug, and many patients will have consumed alcohol
as well. You should try to identify which tablets were taken,
how many and how long ago to establish the likely ongoing
risk and to help plan investigation and treatment.
Try to assess the suicide risk. Features conferring higher
suicide risk are detailed in Box38.1. It is important to cover
the events leading to the overdose, and to try to identify
whether the patient in fact was serious about committing
suicide or whether it represents a cry for help. Evidence that
the act was premeditated suggests that the intention was
suicide (e.g. collecting tablets over a period, a suicide note,
taking tablets when the patient expected to be alone and not
discovered). The actions of the patient after taking the overdose and the course of events leading to hospital admission
are also important. Did the patient ring for help? Ask about
ongoing suicidal ideation and low mood.
RED FLAG
Features indicating a high suicide risk.
• Older age
• Male sex
• Previous suicide attempts
• Unemployed
• Socially isolated (single, living alone)
• Chronic debilitating illness (psychiatric or
physical)
• Drug or alcohol abuse
COMMUNICATION
Patients presenting with deliberate self-harm
or attempted suicide are often challenging and
difficult to engage. If the patient is happy for friends
or family to be present, ensure they are involved.
Input from psychiatrists is also very important.
Examination
The examination should be in three stages: assess how ill
the patient is; look for evidence to suggest the likely drug(s)
involved; and look for complications of overdose.
How ill is the patient?
The priority is ABC – check the airway, breathing and
circulation. The level of consciousness, pulse, blood pressure, temperature and blood glucose level should then be
assessed. When you are assessing the patient’s level of consciousness, use the Glasgow Coma Scale. Ask yourself if the
patient is able to maintain their own airway. Examine the
patient’s pupils, noting the size and reactivity.
Is there any evidence to suggest an underlying cause?
Relatives or ambulance staff may have brought bottles,
packets and boxes from the scene. Look for evidence on
385
Drug overdose and abuse
Table38.1 Specific measures in the management of drug overdose with some of the more common drugs
Drug Toxic side effects Specific management
Opiates Respiratory depression, drowsiness or
Benzodiazepines Drowsiness, dysarthria, nystagmus,
Paracetamol Nausea and vomiting in the first
Aspirin (salicylate) Nausea, vomiting. Salicylate
Digoxin Nausea, vomiting, diarrhoea,
β-Blockers Bradycardia, hypotension, cardiac
Heparin Haemorrhage Protamine sulphate intravenously
Warfarin Haemorrhage Vitamin K intravenously, intravenous infusion of
Tricyclic
antidepressants
CNS, Central nervous system; SVT, supraventricular tachycardia, VT, ventricular tachycardia.
coma, pinpoint pupils, hypotension,
hypothermia, pulmonary oedema
ataxia, coma, respiratory depression
24 h; acute hepatocellular necrosis
may develop after 3days with as
few as 20 tablets causing jaundice,
encephalopathy, hypoglycaemia and
abdominal pain; renal tubular necrosis
may also occur
overdose stimulates the respiratory
centre, resulting in hyperventilation
and respiratory alkalosis. There is
a compensatory renal excretion of
bicarbonate, sodium, potassium and
water, resulting in a metabolic acidosis,
dehydration and electrolyte imbalance.
Acidosis increases the amount that can
cross into the CNS and cause tinnitus,
coma and convulsions
hyperkalaemia, bradyarrhythmias,
tachyarrhythmias, altered colour vision,
delirium
failure, convulsions, coma, asystole
Tachycardia, dry mouth, drowsiness,
mydriasis, increased reflexes, seizures,
coma
Prolonged QT interval may cause VT/
SVT
Naloxone 0.4–2 mg intravenously (may need to be
repeated every 2–3 min to a maximum of 10 mg because
of its short half-life); can be administered by continuous
intravenous infusion
Flumazenil in the case of respiration depression to avoid
the need for intubation. Give 200 μg over 15 s, then 100 μg
every 60 s until response (maximum dose 1 mg); should be
used cautiously. Should be avoided if there is a history of
epilepsy
Monitor blood pressure, prothrombin time, glucose level,
creatinine level and pH and for signs of encephalopathy:
these parameters determine the need for specialist
referral; check paracetamol levels from 4 h onwards
(treatment may begin before a result is available if a
significant overdose is suspected); use a nomogram to
determine whether an antidote should be given if less than
24 h since tablets were taken
Give N-acetylcysteine (Parvolex) by intravenous infusion
Can give repeated doses of activated charcoal. Correct
dehydration, hypokalaemia and hypoglycaemia if
plasma salicylate levels >500 mg/L (3.6 mmol/L), urinary
alkalinization with sodium bicarbonate under close
supervision
In severe poisoning (>700 mg/L or 5.1 mmol/L),
haemodialysis may be life-saving
Correct electrolyte disturbance
Temporary ventricular pacing in atrioventricular block
Digoxin-specific antibody fragments (Digibind) in severe
overdose
Atropine intravenously for bradycardia
Glucagon intravenously in severe overdose
concentrates of prothrombin and factor VII, IX and X, or
fresh frozen plasma
Supportive measures; special attention to acidosis and
hypoxia
Treat seizures and delirium with lorazepam or diazepam
Sodium bicarbonate if significant overdose
the patient such as diabetic cards (e.g. insulin overdose) or
hospital appointment cards or MedicAlert bracelets. The
hospital's electronic system may alert you to the patient’s
last prescription and if the patient has taken overdoses previously. Also look for:
• pinpoint pupils: opiates, organophosphates;
• dilated pupils: tricyclic antidepressants, amphetamines,
cocaine, γ-hydroxybutyrate;
• nystagmus: phenytoin, alcohol;
386
• burns around the mouth: corrosives;
• hyperventilation: aspirin;
• needle marks: opiates, benzodiazepines,
stimulants.
Have any complications occurred?
Box 38.3 summarizes complications of drug overdose. A
low-reading thermometer is necessary to properly detect
and assess hypothermia.
Common presentation, investigations and management
3838
Table38.2 Features and management of common illegal
drug overdose
Substance Clinical features Management
Heroin and other
opioids (smack,
junk, gear, horse)
Cocaine/crack
cocaine (coke,
charlie, snow)
Ketamine (K,
special K)
Mephedrone
(miaow miaow,
M-cat)
γ-Hydroxybutyrate Euphoria,
MDMA/
amphetamines
(ecstasy, speed,
pills)
See Fig.39.1 See Fig.39.1
Euphoria,
tachycardia,
agitation,
hyperthermia,
coronary artery
spasm, seizures,
acidosis
Dissociation,
hypertension,
arrhythmia,
respiratory
depression
Agitation,
tachycardia,
hypertension,
seizures
dizziness,
hypotonia,
bradycardia,
respiratory
depression
Agitation,
tachycardia,
psychosis,
hyperthermia,
rhabdomyolysis
Sedation, active
cooling, glyceryl
trinitrate.
β-Blockers are
contraindicated
Supportive
measures
Supportive
measures
Supportive
measures.
γ-Hydroxybutyrate
is rapidly
metabolized and
cleared
Supportive
measures,
sedation,
β-blockers
RED FLAG
Complications of drug overdose:
• coma
• respiratory depression
• hypotension or hypertension
• arrhythmias
• seizures
• head injury
• hypothermia or hyperthermia
• aspiration pneumonia
• rhabdomyolysis (can cause renal failure)
• organ failure
• gastric stress ulceration
Investigations
• Paracetamol and salicylate levels should be measured in
all patients. If you can establish the timing of ingestion,
levels should be measured as close to 4 hours after
ingestion if possible.
• Urea and electrolyte levels (including magnesium),
blood glucose level, serum osmolarity, creatine kinase
level.
• Baseline clotting and liver function tests in paracetamol
overdose.
• Drug levels can be measured in the blood, gastric
contents and urine. Arterial blood gas to assess
respiratory depression or stimulation (opiates,
salicylate) and acid–base status.
• Electrocardiogram is advisable in all patients, as many
drugs can cause arrhythmia in overdose.
• Chest X-ray: if evidence of aspiration.
• If the patient is unconscious, consider further imaging
to rule out an intracranial event.
Management
The management of drug overdose can be divided into three
parts: general supportive measures for all patients; specific
measures according to the drug taken; and psychiatric assessment and social input when the patient recovers physically.
Supportive care
• If the patient is unconscious, assess the airway and give
oxygen via a face mask.
• If the patient is not maintaining an airway, call an
anaesthetist as the patient may need intubation.
• Some patients may require assisted ventilation.
• Maintain blood pressure with intravenous fluids as
required.
• Measure clinical observations including oxygen
saturations, pulse rate, blood pressure, temperature,
neurological status (Glasgow coma scale), and glucose level
regularly – patients who seem well may deteriorate rapidly.
• Attach a cardiac monitor if arrhythmia is suspected
or the patient is known to have taken tricyclic
antidepressants or other medications known to cause
cardiac instability (e.g. β-blockers, digoxin).
• In arrhythmia, correct hypoxia, acidosis or electrolyte
imbalance; antiarrhythmic agents should be used with
caution as they can exacerbate the arrhythmia.
• Convulsions should be treated with intravenous
benzodiazepines.
Preventing absorption
If recommended by protocol or a poisons advice service, activated charcoal may be used to bind poisons in the stomach
to prevent their absorption.
• It is more effective the sooner it is given, and usually
needs to be given within 1 hour of ingestion.
• Repeated doses are not routinely recommended but may
be indicated in cases of tricyclic and aspirin overdose.
• It is contraindicated in drowsy patients (risk of
aspiration). The administration of activated charcoal
is associated with aspiration and gastrointestinal
obstruction.
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