Cocaine Use Disorder

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Cocaine use\: causes 850 deaths per year in the UK; used by 2.5% of adults aged 16-59.
Aetiology\: stimulant that acts on the sympathetic nervous system, causing a sympathomimetic toxidrome.
Risk factors\: male, impulsivity, genetic predisposition, mental health conditions, childhood trauma, lower socioeconomic
group, poly-substance use.
Symptoms\: agitation, hallucinations, euphoria, headache, palpitations, convulsions, chest and abdominal pain.
Signs\: tachycardia, dysrhythmias, hypertension, tachypnoea, mydriasis, hyperpyrexia.
Investigations\: ECG, urine toxicology, FBC, U&E, liver function, CK, bone pro
Management\: supportive, IV
Complications\: arrhythmias, seizures, rhabdomyolysis, methaemoglobinaemia, vasculitis, AKI, bladder cancer.
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Introduction

Cocaine use causes around 850 deaths per year in the UK, with 2.5% of adults aged 16-59 using the drug each year.
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Cocaine can be taken through a variety of routes, including oral, intravenous, intranasal or inhalation.
Cocaine may be diluted with other substances, which vary throughout regions, including lidocaine, phenytoin, and
levamisole (anti-parasitic medication). This can a
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Aetiology

Cocaine is a stimulant drug that acts on the sympathetic nervous system, causing a sympathomimetic toxidrome. It is
produced from E r y t h r o x y l o n coca leaves, native to South America.
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It causes widespread vasoconstriction by inhibiting noradrenaline reuptake and increasing alpha and beta receptor
stimulation. Cocaine blocks voltage-gated sodium channels, thus stopping the depolarisation of nerve
local anaesthetic e
euphoric and addictive properties.
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Its peak plasma concentration varies depending on the administration route; with intravenous (IV) use, this peaks within
minutes. Cocaine has a short half-life of roughly one hour. Cocaine use in the presence of alcohol creates a cardiotoxic
metabolite called cocaethylene, which has a longer half-life.
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Risk factors

Risk factors for cocaine use include\:
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Male
Impulsivity
Genetics\: higher risk if one or both parents use cocaine
Co-existing mental health conditions\: depression, ADHD and anxiety
Childhood traumaLower socioeconomic group
Poly-substance use

Clinical features

History
Typical symptoms of cocaine use include\:
Agitation
Hallucinations
Euphoria
Headache
Palpitations
Convulsions
Nausea and vomiting
Sweating
Chest pain
Abdominal pain
Clinical examination
Typical clinical
Tachycardia and dysrhythmias
Hypertension
Tachypnoea
Mydriasis (dilated pupils)
Hyperpyrexia

Di

There are many di
Di
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Hypoglycaemia
Intracerebral haemorrhage
Acute psychosis
Delirium tremens
Thyrotoxicosis
Other substances can also produce a sympathomimetic toxidrome, including\:
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Amphetamines
Methamphetamines
LSD
MDMA
Table 1. Toxidromes and their causes.
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Heart rate Respiratory rate Pupils Temp Skin Mental state
Sympathomimetic
(Cocaine)
Anticholinergic
(Antihistamines)
Cholinergic
(Organophosphates)
Raised Raised Dilated Raised Diaphoretic Agitated
Raised No change Dilated Raised Dry Confused
Reduced No change Pinpoint No change Diaphoretic ConfusedOpioid
(Heroin)
Sedative
(Benzodiazepines)
Reduced Reduced Pinpoint No change No change Depressed
Reduced Decreased No change No change No change Depressed

Investigations

Bedside investigations
Relevant bedside investigations include\:
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Basic observations\: to assess for tachycardia, tachypnoea, and hypertension
ECG and cardiac monitoring\: to detect and monitor dysrhythmia
Blood glucose\: to exclude hypoglycaemia
Urine toxicology screen\: to determine if other substances have been used
Laboratory investigations
Relevant laboratory investigations include\:
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Full blood count\: to exclude agranulocytosis
Urea and electrolytes\: may be deranged in acute kidney injury
Liver function tests\: may be deranged in hepatic injury
Creatinine kinase\: raised in rhabdomyolysis
Bone pro\: calcium disorders may cause seizures
Magnesium\: magnesium disorders may cause seizures
Coagulation screen\: to monitor coagulation in bleeding
Arterial blood gas\: for acid-base disturbances and methaemoglobinaemia
Serial troponin\: raised in myocardial ischaemia
Autoantibodies\: if ANCA-associated vasculitis is suspected to be caused by cocaine
Imaging
Imaging should be guided by clinical judgement and requested depending on clinical features. Relevant imaging may
include\:
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Chest X-ray\: if chest pain/dyspnoea, to exclude pneumothorax, pneumomediastinum etc.
CT head\: if neurological symptoms, to exclude intracranial haemorrhage as a di

Management

There is no antidote for cocaine; therefore, management is supportive and to treat associated complications. An ABCDE
approach should be used for those presenting with acute cocaine use.
If a patient is agitated, aim to de-escalate the situation by using a quiet room, open body language, and, if possible,
involving friends/family if it is safe to do so. If this fails, assess capacity and consider whether pharmacological sedation
would be in the patient's best interests.
If more information is required after escalation to a senior, call the local poisons information service.
Initial management
The medical management of cocaine use depends on the presentation and associated complications.
Initial management may include\:
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Activated charcoal\: considered if presenting within 1 hour of oral ingestion with no airway compromise
IV \: patients may be
disturbances
Sedation\: benzodiazepines (lorazepam or diazepam) are preferred, with haloperidol as an adjunct if required
Cooling\: misting, ice packs and fanning. If temperature > 38.5°C, urgent invasive cooling is required (e.g. cold
and ice baths)Ongoing management
Patients should be osubstance misuse service and psychiatry liaison team.
There should be at least 4 hours of observation after the last known exposure to cocaine. This should include cardiac
monitoring with heart rate, blood pressure, consciousness level and temperature. Asymptomatic, stable patients can be
discharged with safety netting advice to return to the emergency department if they become symptomatic.
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Mental Capacity Act
Patients may present with agitation, delirium, hallucinations, or reduced GCS, all of which could impact their ability to make
decisions.
During the consultation, it's important to assess the patient’s capacity. Capacity is decision and time speci
important to cover decisions to refuse treatment and self-discharge.
A patient should be assumed to have capacity until proven otherwise. If there is doubt, their capacity should be assessed.
To have capacity to make a speci
1. Understand the information given
2. Retain the information
3. Weigh up the risks and bene
4. Communicate their decision

Complications

Cocaine use causes multi-organ disease. A thorough history, systemic review and examination should be conducted, and
complications managed accordingly.
Cardiovascular
Due to coronary vasoconstriction/vasospasm, patients may present with acute coronary syndrome and aortic dissection.
Cocaine-induced chest pain is investigated like any other chest pain. Unlike atherosclerotic ischaemia, in this patient group,
benzodiazepines can be used.
Tachyarrhythmias such as ventricular supraventricular tachycardia should be
managed according to adult life support guidelines.
Patients may develop hypertension as a result of cocaine use. If there is uncontrolled hypertension causing end-organ
damage, then IV glyceryl trinitrate (GTN) or nifedipine can be used.
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Neurological
Seizures lasting longer than 5 minutes or refractory seizures (two or more within a 5-minute period without recovery of
consciousness between) are managed as status epileptics with benzodiazepines such as midazolam, diazepam or
lorazepam.
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Haematological
Methaemoglobinaemia and agranulocytosis can occur due to substances diluted with cocaine.
Methaemoglobinaemia is caused by the oxidation of ferrous iron to ferric iron within the haem component of haemoglobin.
It can be detected with an arterial blood gas, with a discrepancy between PaO 2 2
and SpO . The signs and symptoms depend
on its concentration and can range from cyanosis, dyspnoea, and headache to seizures, dysrhythmias, coma, and death.
Treatment is with high-
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Rhabdomyolysis may occur and can present with muscle aches, weakness, fatigue, and vomiting. Treatment is with IV
hyperkalaemia).
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The most common acid-base disorder is a high anion gap metabolic acidosis, which can typically be managed with IV

monitored with serial blood gases, with a low threshold for critical care involvement.
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Urological/renal
Cocaine can cause acute and chronic kidney disease. With chronic use, there is an increased risk of bladder cancer.
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If cocaine is diluted with levamisole, there is an increased risk of vasculitis, including granulomatosis with polyangiitis and
midline destructive vasculitis. The latter presents with the destruction of the nasal cartilage, leading to perforation due to a
combination of vasoconstriction, trauma from cocaine crystals, and recurrent nasal infections.
10References
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Reviewer

Dr Charlotte-Leigh Ibbetson
Consultant in Emergency Medicine

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Contents

Introduction
Aetiology
Risk factors
Clinical features
Source\: geekymedics.com