Drug group	Examples
Alcohols	Ethanol, methanol, isopropyl glycol, ethylene glycol
Metals	Lithium, iron, mercury, potassium, lead, arsenic
Acids and alkalis
Hydrocarbons	Turpentine, kerosene, eucalyptus oil, benzene

Elimination

There are several forms of enhanced elimination that are more commonly used depending on the type of overdose. Again, assess the severity of the toxicity to determine whether employing these techniques will be beneficial.

Multiple doses of charcoal may decrease drug absorption in some cases (Box 28.2). A suggested dosing regimen would be 25 g (adults) or 0.5 g/kg (children) every 2–4 hours. It is contraindicated if there is a bowel obstruction or decreased level of consciousness in a patient without a protected airway. Always check for the presence of bowel sounds before administering the next dose.

Box 28.2 Situations when multiple doses of charcoal may reduce drug absorption

Ingestion involves large amounts or formation of concretions/bezoars.

Drugs are enteric-coated or slow-release.

Reabsorption (e.g. via enterohepatic circulation) can be prevented.

Stomach emptying is delayed (e.g. anticholinergic effects). Ensure the presence of bowel sounds prior to repeating dose of charcoal as ileus can occur due to anticholinergic effects.

The drug involved is carbamazepine, dapsone, phenobarbitone, quinine or theophylline.

Urinary alkalinisation may be used for increasing elimination of weak acids. This can be achieved by intravenous administration of sodium bicarbonate. Give a bolus of 1 mmol/kg IV followed by an infusion (100 mmol of sodium bicarbonate in 1000 mL 5% dextrose in 0.9% saline over 4 hours). Adjust the rate to a urinary pH > 7.5. Complications of bicarbonate therapy include fluid overload, alkalaemia, hypokalaemia and hypocalcaemia. Main indication is salicylate overdose.

Whole bowel irrigation with agents such as polyethylene glycol is rarely used. It hastens the elimination of poorly absorbed or slow-release medications before they can be absorbed. Complications include vomiting, abdominal bloating and pain. Rarely colonic or oesophageal perforation has been reported as well as GI bleeding (Mallory-Weiss tear) and aspiration pneumonia after vomiting.

Dialysis is the most commonly used form of extracorporeal elimination. It can enhance elimination of various toxins (Box 28.3). Indications for dialysis are listed in Box 28.4.

Box 28.3 Drugs amenable to dialysis

Box 28.4 Indications for dialysis

Failure to respond to full supportive methods

Inability to excrete or metabolise drug due to impaired route of elimination (e.g. renal failure, hepatic failure)

Associated metabolic abnormalities that would be resolved with dialysis (e.g. metformin lactic acidosis)

Specific therapies

Coma

• Reduced GCS is a common toxic effect of many drugs and poisons.

• Look for reversible causes and treat urgently—hypoglycaemia, opiate intoxication.

• Priority is focused on establishing a patent and finally a protected airway.

• If coma was not a predicted outcome of the overdose investigate for other causes.

Seizures

• Benzodiazepines are first-line therapies for drug-related seizures.

• Barbiturates are second-line.

• Phenytoin is not indicated.

• If seizures are atypical (focal or partial), further investigation of the seizure is warranted.

Cardiovascular instability

• Management of hypotension involves intravenous access and fluids. Treat any associated arrhythmias.

• Antidotes, specific therapies and inotropes may be indicated (calcium for calcium-channel blocker overdose, sodium bicarbonate for tricyclic, antidepressant overdose, inotropes for beta-blocker overdose).

Hyperthermia

• Hyperthermia has life-threatening consequences such as multi-organ failure.

• Aggressive early treatment is essential.

• Cooled fluids, cooling blanket ± intubation, ventilation and paralysis are among the treatment options.

• Continuously monitor core temperature (rectal/bladder).

Metabolic and cognitive disturbances

• Screen for and treat conditions such as hypoxia, hypercarbia, glucose and acid–base and electrolyte abnormalities.

• Manage agitation and confusion initially with verbal reassurance and if unsuccessful use benzodiazepines (first-line) or olanzapine to achieve gentle sedation. Key aims include safety of the patient (prevention of absconding) and safety of the staff.

Antidotes

For a list of antidotes, see the ‘Quick reference’ section.

TOXIDROMES AND SPECIFIC OVERDOSES

The clinical presentation of some poisonings may be predictable based on the pharmacology of the drug/substance involved. Some classic toxidromes with examples are listed in Table 28.2.

Table 28.2 Some classic toxidromes

Benzodiazepines

Overdoses of benzodiazepines are common and have a good prognosis with supportive treatment. CNS and respiratory depression are the main toxic effects. Flumazenil may confirm the diagnosis but is generally not used for treatment, unless reversing iatrogenic conscious sedation or if advanced airway management is unavailable. The half-life of flumazenil (about 1 hour) is much shorter than that of all benzodiazepines; repeat doses of flumazenil may be required to maintain effect.

Key points—benzodiazepines

• Use flumazenil carefully in mixed overdoses as some co-ingestants (e.g. tricyclic antidepressants) may be proconvulsant and flumazenil may precipitate seizures and death.

• Other contraindications include known seizure disorder and benzodiazepine dependence.

Opioids

This group of drugs includes those derived from opium as well as those that have opiate-like activity. Typical toxic effects are CNS and respiratory depression and miosis. Acute lung injury has been reported, typically occurring once ventilation has been restored following a period of respiratory depression. Other effects include mild hypotension (arteriolar and venous vasodilation). Treatment of opioid toxicity is supportive, especially of the airway and ventilation, and sometimes involves the use of naloxone, either as bolus dose(s) or infusion. Several drugs in this group have atypical toxic effects (Table 28.3).

Table 28.3 Atypical opioids

Opioid	Atypical toxic effects of clinical significance
Tramadol	Serotonergic syndrome, seizures
Dextropropoxyphene	Seizures, wide QRS arrhythmias, negative inotropic effects (Na channel blockade)
Methadone	Prolonged QT interval (possibly → torsades de pointes)
Pethidine	Seizures
Fentanyl	Muscle rigidity (rapid injection)

Key points—opioids

• Check the duration of action of the opioid involved. Some are as short as several hours (fentanyl, heroin) and others as long as 24 hours (methadone and controlled-release forms of morphine and oxycodone). This may help to predict the likelihood of requiring a naloxone infusion and intensive care.

• Be mindful of more unusual routes of opioid administration such as transdermal patches (fentanyl).

• Naloxone can be life-saving. The treatment goal is adequate respiration as opposed to complete CNS recovery. Infusions can be used for the longer acting opioid intoxication.

• The effects of naloxone are seen within minutes when administered intravenously. Duration of action is short (0.5 hours). Depending on the opioid, observation for up to 12–24 hours after receiving naloxone may be required, as administration of the antidote may need to be repeated.

• Naloxone can precipitate severe opioid withdrawal in the tolerant patient. Reverse respiratory depression with small increments in order to prevent severe withdrawal.

• Buprenorphine is a partial agonist. In overdose, naloxone can be used to reverse respiratory depression but a partial or complete lack of response may be seen.

Paracetamol

Paracetamol overdoses can be either single or staggered ingestions. There are four described stages of paracetamol poisoning (Table 28.4). Stage II marks the onset of liver injury. Renal failure is seen in 25–50% of those with hepatic dysfunction. Death is usually due to multi-organ failure, sepsis, haemorrhage, acute respiratory distress syndrome and/or cerebral oedema. Key blood tests are paracetamol level and transaminases—aspartate aminotransferase (AST) and alanine aminotransferase (ALT). Prothrombin time (PT) may also be indicated. Paracetamol levels are reported in various units (mg/L or μmol/L). When plotting the paracetamol level on the nomogram, always check the units are corresponding to the correct axis. Failure to do so may be life-threatening.

Table 28.4 Stages of paracetamol poisoning

Paracetamol can be implicated in an accidental overdose. Remember to ask quantities of paracetamol ingested in the patient who has been self-medicating to achieve analgesia. Paracetamol is a common component of over-the-counter medications such as cold and flu preparations and migraine tablets. Serious hepatotoxicity is less common in children compared to adults. Charcoal can be given in those who present within 1 hour after potentially toxic ingestions.

Key points—paracetamol

• Presentation > 8 hours after ingestion increases the likelihood of hepatic failure and death.

• N-acetylcysteine (NAC) should be commenced immediately if:

• time of ingestion is unknown

• there are signs of hepatic injury after any paracetamol overdose.

• Do not delay commencing NAC if > 8–24 hours after ingestion. The infusion can be ceased or continued once the paracetamol level and results of transaminases are analysed.

• Hepatotoxicity is unlikely if > 24 hours after ingestion has elapsed and transaminases are normal and paracetamol is undetectable.

• Guidelines for sustained-release products. If the total dose ingested is > 150 mg/kg start NAC immediately and take 4- and 8-hour paracetamol levels. Only cease NAC if both levels are below the line on the nomogram.

• Serial LFTs and PT are recommended in cases where NAC has been commenced in patients presenting 8 hours after ingestion.

• Increases in AST and ALT levels are frequently the first laboratory sign of liver injury in paracetamol toxicity. Hepatotoxicity is defined as an AST or ALT > 1000 IU/L. King’s College Criteria for paracetamol toxicity are predictors of poor prognosis. They are:

• pH <7.3 after adequate fluid resuscitation

• creatinine > 300 μmol/L

• prothrombin time > 100 seconds or international normalised ratio (INR) > 6.5

• grade III or IV encephalopathy.

• Early referral or consultation with liver transplantation services should be considered if any of the King’s College Criteria are present or worsening serial tests (↑ PT/INR or creatinine, ↓ pH and severe thrombocytopenia).

Guidelines and treatment nomogram

A recent collaboration of clinical toxicologists in Australia and New Zealand resulted in new guidelines and a new treatment nomogram published in the Medical Journal of Australia (March 2008). These are summarised below.

General key points

• There is a new treatment nomogram which lowers the old nomogram by 25%.

• Possible toxic doses:

• As a guide, > 200 mg/kg or 10 g (whichever is less) of paracetamol either as a single ingestion or staggered over a single 24-hour period in adults or children > 6 years may be associated with hepatic injury.

• As a guide, ≥ 200 mg/kg of paracetamol either as a single ingestion or staggered over a single 24-hour period in children aged 0–6 years may be associated with hepatic injury.

Management of acute single ingestions

Paracetamol levels measured > 4 hours post-ingestion can be plotted on a nomogram to determine risk of hepatotoxicity and indicate the need for N-acetylcysteine (NAC) therapy.

Presentation within 8 hours:

1. Measure the serum paracetamol (at 4–8 hours) and plot according to the nomogram. No other tests (e.g. LFTs, INR) are beneficial in making a risk assessment.

2. If the level is plotted above the treatment line, commence and complete NAC therapy. No further tests are required following completion of 20-hour NAC infusion.

3. If the level is plotted below the treatment line, then no further medical treatment is required.

Presentation 8 hours after ingestion:

1. NAC should be commenced immediately if:

• the reported dose is possibly toxic (see above)

• the patient shows signs of hepatic injury (nausea, vomiting, right upper quadrant pain or tenderness).

2. Measure serum paracetamol level and ALT.

• If the paracetamol level plots under the treatment line and the ALT is normal, stop NAC.

• If the paracetamol level plots under the treatment line and the ALT is raised, continue NAC. Measure ALT after completion of NAC. If ALT is normal, no further treatment is required. If ALT is abnormal, continue NAC and measure INR and platelet count.

• If the paracetamol level plots above the treatment line on the nomogram, continue NAC treatment and remeasure the ALT at the end of the infusion. If the ALT is normal, nothing further is required. If the ALT is raised, continue NAC and monitor INR and platelet count.

Management of staggered ingestions

• If it has been less than 8 hours since the first dose, treat as above (acute single ingestion presenting within 8 hours).

• If it has been more than 8 hours since the first dose, treat as above (acute single ingestion presenting after 8 hours).

Repeated supratherapeutic ingestion

1. If patient has ingested a possible toxic dose (see Table 28.5), measure serum paracetamol level and ALT.

2. If ALT is normal and the paracetamol level < 120 μmol/L (20 mg/L), no further treatment is required.

3. If there is any other result, commence NAC and repeat paracetamol level and ALT at 8 hours. If ALT is normal or static, no further treatment is required; if ALT is abnormal or worsening, continue NAC and check ALT at 12-hourly intervals.

Table 28.5 Repeated supratherapeutic doses that may be associated with hepatic injury

Adults and children aged > 6 years	Children aged < 6 years
> 200 mg/kg or 10 g (whichever is less) over a single 24-hour period	≥ 200 mg/kg over a single 24-hour period
150 mg/kg or 6 g (whichever is less) per 24-hour period for the preceding 48 hours	≥ 150 mg/kg per 24-hour period for the preceding 48 hours
> 100 mg/kg or 4 g/day (whichever is less) in patients with predisposing risk factors (e.g. chronic alcohol use, use of enzyme-inducing drugs, prolonged fasting, dehydration)	≥ 100 mg/kg per 24-hour period for the preceding 72 hours

Sustained-release paracetamol

1. If > 200 mg/kg or 10 g (whichever is less) has been ingested, commence NAC.

2. Measure serum paracetamol level at 4 hours post-ingestion and then again 4 hours later if the first level was below the treatment line.

• If both levels are below the line, NAC can be stopped.

• If either level is above the line, continue NAC as per the guidelines under ‘acute single ingestions’.

Key points—N-acetylcysteine (NAC)

• NAC reduces the incidence of hepatotoxicity, hepatic failure and mortality in patients who present with normal liver function in the context of known ingestions.

• Adverse reactions include nausea and vomiting, anaphylactoid-type of reactions—mainly cutaneous. Treatment of these reactions includes stopping the infusion, administering antihistamines and recommencing the infusion at a slower rate. Bronchospasm, hypotension and angio-oedema have uncommonly been reported (< 2%).

• NAC has been shown to be useful even in late presentations with evidence of fulminant hepatic failure (decreases cerebral oedema, mortality). However efficacy decreases the longer the delay beyond 8 hours post-ingestion.

Illicit drugs

The majority of these are best divided into stimulants versus depressants (Tables 28.6 and 28.7). The others can be classed as hallucinogens (Table 28.8). Amyl nitrite is considered alone.

Table 28.6 Stimulants

Drug name	Common street names
Cocaine	Coke
Methylenedioxymethamphetamine (MDMA)	Ecstasy
Methamphetamine (MDA)	Ice, speed
Para-methoxyamphetamine (PMA)	Red mitsubishi^∗, Dr Death
Para-methoxymethylamphetamine (PMMA)
4-methylthioamphetamine (4-MTA)	Flatliner

∗ Not all pills with the red mitsubishi logo contain PMA.

Table 28.7 Depressants

Drug name	Common street names
Heroin
Gamma-hydroxybutyrate	G, GBH, fantasy, grievous bodily harm
Ketamine	Special K

Table 28.8 Hallucinogens and others

Hallucinogens	Others
Cannabinoids LSD (‘acid’)	Amyl nitrite (‘poppers’)

Stimulants

Cocaine and the amphetamines act via stimulation of the central and peripheral adrenergic receptors. They are sympathomimetic agents. The most common clinical effects of this group of drugs are outlined in Table 28.9.

Table 28.9 Clinical effects of cocaine and the amphetamines

System	Clinical effect
CNS	Hallucinations (tactile, visual) Agitation Anxiety Psychosis Euphoria Seizures Tremor

Cardiovascular

Tachycardia

Hypertension

Chest pain (acute coronary syndrome)

Arrhythmias (mainly cocaine)

Other

Cocaine

• Cocaine has additional properties—it blocks sodium channels, is thrombogenic by promoting platelet aggregation and is vasospastic. It can also accelerate atherosclerosis.

• Cocaine is more likely than amphetamines to cause seizures, arrhythmias and myocardial ischaemia.

• Atypical chest pain is the norm for presentations of myocardial ischaemia so a high index of suspicion must be maintained.

• Use up to 4 days prior to presentation may be responsible for symptoms due to longer lasting toxic metabolites.

Amphetamines (MDMA, MDA, PMA, PMMA, 4-MTA)

• These are more hallucinogenic due to their greater dopaminergic effect.

• MDMA has been known to cause hyponatraemia and serotonin syndrome; therefore exercise caution in the delirious or post-ictal patient who has taken Ecstasy.

• Hyponatraemia secondary to MDMA is thought to arise through several mechanisms—syndrome of inappropriate anti-diuretic hormone (SIADH), water intoxication and loss of sodium in sweat (high ambient nightclub temperatures and dancing).

• Serotonin syndrome (Table 28.10) can be life-threatening and is diagnosed clinically according to features from three categories—autonomic, neuromuscular and central nervous system abnormalities. Management is supportive and, if hyperthermic, early active cooling usually in association with intubation and paralysis is essential.

• ‘Ice’ is a growing trend in Australia. The most common clinical presentation features aggression, paranoia, psychosis and agitation. The mainstay of treatment is sedation—options include benzodiazepines and antipsychotics (olanzapine, haloperidol). The route of administration of the sedatives will depend on the clinical state of the patient and level of cooperation. Most cases are so severe that parenteral rapid sedation is the only management. Sedation may need to be maintained until the effects of the amphetamine have ceased.

• PMA and PMMA are more potent than MDMA but with a slower onset of action. Because of this, people tend to take more and consequently overdose. They are often sold as ‘red mitsubishi’ tablets or even as Ecstasy. They have been linked to deaths around the world, including Australia. Toxicity and death have been attributed to hyperthermia, rhabdomyolysis, seizures, disseminated intravascular coagulation, intracerebral haemorrhage or infarction, cardiac arrhythmias, electrolyte disturbances and multi-organ failure.

• 4-MTA has a mild stimulant effect, less hallucinogenic and less euphoric compared with MDMA. It has been linked to multiple deaths in Europe though it is probably only lethal in excess or in combination with other drugs such as MDMA and cocaine.

Table 28.10 Clinical features of serotonin syndrome

Autonomic dysfunction	Neuromuscular dysfunction	CNS dysfunction
Hyperthermia	Myoclonus	Confusion
Diaphoresis	Hyperreflexia	Disorientation
Sinus tachycardia	Muscle rigidity	Agitation
Hypertension	Tremor	Coma
Hypotension	Hyperactivity	Anxiety
Tachypnoea	Ataxia	Hypomania
Dilated pupils	Shivering	Lethargy
Unreactive pupils	Seizures	Insomnia
Flushed skin	Nystagmus	Hallucinations
Diarrhoea	Teeth chattering	Dizziness

Key points—stimulants

• Benzodiazepines are the treatment of choice for CNS and some cardiovascular (tachycardia, hypertension) effects of cocaine and amphetamine toxicity.

• Second-line therapies for hypertension include glycerol trinitrate or sodium nitroprusside infusions. Beta-blockers are contraindicated.

• Beta-blockers are contraindicated in the treatment of cocaine toxicity due to potential for unopposed alpha stimulation. This can result in increased blood pressure, reduced coronary blood flow and reduced left ventricular (LV) function and reduced cardiac output.

• Management of chest pain in the context of cocaine or amphetamines is as with the usual work-up for acute coronary syndromes. An ECG, CXR and cardiac markers must be obtained and other causes for chest pain (e.g. dissection) should be ruled out. Aspirin, nitrates and diazepam should be given. The dose of diazepam is titrated to gentle sedation and the heart rate, aiming for settling of tachycardia (to reduce myocardial oxygen demand).

• Ventricular tachyarrhythmias due to cocaine toxicity should be initially treated with sodium bicarbonate.

• Do not assume altered mental state or seizures are merely drug effects. Always exclude hyponatraemia as a cause. It is a life-threatening condition that can be treated and often requires intensive care.

• Aggressive early management of hyperthermia is crucial. Cooled fluids, cooling blanket and intubation, ventilation and paralysis (to prevent heat generation through shivering) are treatment options.

• Ecstasy may not be MDMA. It may contain any of the methamphetamines.

Depressants

Gamma-hydroxybutyrate (GHB) and analogues

This group of drugs consists of GHB, gamma-butyrolactone and 1,4 butanediol. They exhibit similar clinical effects. GHB was initially developed as an anaesthetic agent in the 1960s. It is a clear, colourless and reasonably tasteless drug with minimal ‘hangover’ effect which makes it palatable to the user and also accounts for it being implicated sometimes as a ‘date rape’ drug. The most prominent clinical feature of toxicity is a rapid onset of coma, often to a GCS as low as 3 (Box 28.5). Varying GCS over a short period of time can also occur. For example, a patient can oscillate from GCS 6 to 10 and then back to 6 in a period of 15–30 minutes. This phenomenon typically occurs as the drug effects are subsiding.

Box 28.5 Clinical features of GHB intoxication

Decreased GCS (often coma)

Due to the rapid onset and short duration of action, there is no role for decontamination. Treatment is supportive and care must be taken with the intubated patient, as rapid recovery and violent arousal can result in self-extubation. Emergence delirium is often seen in the recovery phase.

Key points—GHB

• Patients have a good outcome with supportive care including intubation and ventilation.

• GHB has an accumulative effect with repeated dosing and an additive effect with other CNS depressants such as alcohol and benzodiazepines.

• The drug has a short duration of action, with most patients recovering within 2–6 hours.

• Patients who are not improving should be further investigated (e.g. CT scan of brain).

Ketamine

This is a dissociative anaesthetic agent. It is often swallowed, snorted or injected but can also be smoked. Users feel detached from their immediate surroundings, have ‘out-of-body’ experiences (flying, floating) and hallucinate. They do not respond to stimuli in their external surroundings. It is generally short-acting and fatalities are rare.

• Hypoventilation is uncommon.

• Effects can vary from appearing inebriated to being calm or agitated or violent. With larger doses, incoordination, inability to speak and confusion are common.

• Dystonic reactions, myoclonus, tremor and muscle rigidity can occur.

• Hypertension, tachycardia and bronchodilatation are often seen.

• In overdose, coma occurs.

• Treatment options depending on the clinical setting include supportive care, sedation (benzodiazepines) and advanced airway management.

Hallucinogens

Cannabinoids

• Cannabinoids refers to active substances from Cannabis sativa. Cannabinol, cannabidiol and tetrahydrocannabinol are the major substances of this group. The principal psychoactive cannabinoid is Δ⁹-tetrahydrocannabinol (THC).

• Marijuana is the name for a mixture of dried leaves and flowers of the plant.

• Hashish is the pressed resin. Hashish oil is the oil from hashish.

• The concentration of THC varies from 1% in low-grade marijuana up to 50% in hash oil.

• These substances may be smoked or ingested. Effects are apparent within minutes of smoking, and from 1–3 hours after ingestion.

• Clinical effects are listed in Table 28.11.

• Life-threatening toxicity is rare. The mainstay of treatment is supportive with reassurance and benzodiazepines and/or occasionally antipsychotics (e.g. olanzapine) for gentle sedation in the agitated, paranoid or psychotic patient.

Table 28.11 Clinical effects of cannabinoids

Psychological

Relaxation

Sense of wellbeing

Increased sensory awareness

CVS

CNS

Decreased muscle strength

Psychiatric

Lysergic acid diethylamide (LSD)

• This is a synthetic hallucinogen which is able to alter and distort perception, thought and mood.

• It is generally sold as liquid-impregnated blotter paper or microdots and ingested. The onset of effects after ingestion is usually within 30–60 minutes, lasting approximately 10–12 hours.

• Auditory and visual hallucinations and size, shape and colour distortions may occur, as well as synaesthesia, a crossing over of the senses often described as ‘hearing colours’ or ‘seeing sounds’.

• Potentially life-threatening complications include hyperthermia, coma, respiratory arrest, hypertension, tachycardia and coagulopathy but have only been described in patients following a massive LSD overdose. Serotonin syndrome has been described with LSD use.

• Diagnosis relies on detection of the presence of methaemoglobinaemia on co-oximetry.

• Treat symptomatic patients with methylene blue 1–2 mg/kg IV over 5 minutes. Consider treating the asymptomatic patient with methaemoglobin levels > 20%. Response should be apparent within 30–60 minutes. If not or insufficient, the dose may be repeated.

• Monitor with serial methaemoglobin levels.

Table 28.12 Clinical effects of methaemoglobinaemia

% Methaemoglobinaemia	Clinical features
10–20%	Cyanosis
20–50%	Shortness of breath (SOB), dizziness, fatigue, headache
> 50%	Tachypnoea, lethargy, coma, seizures, death

Beta-blockers

• Toxicity may occur with relatively small doses.

• Of all the available beta-blockers, propranolol or sotolol toxicity are the most clinically significant and may be life-threatening.

• Clinical manifestations are usually apparent by 4 hours (Table 28.13).

• ECG changes include:

• PR prolongation (early indicator of toxicity)

• QRS widening

• QT prolongation.

Table 28.13 Clinical features of beta-blocker overdose

Cardiovascular

CNS

Respiratory

Metabolic/endocrine

Hypoglycaemia

Hyperglycaemia

Hyperkalaemia

Management

1. Continuous cardiac monitoring is essential and invasive blood pressure monitoring may also be required.

2. Glucagon is the classic antidote but its use is often limited by availability. Other inotropes are good substitutes.

3. Treatment of bradycardia and hypotension includes atropine, adrenaline, isoprenaline and glucagon.

4. Give sodium bicarbonate for wide QRS and ventricular arrhythmias (as with TCA overdose).

5. Remember slow release preparations exist.

Calcium channel blockers

The centrally acting calcium channel blockers (Table 28.14) are the most cardiotoxic in this group and effects can be delayed (up to 16 hours) due to the sustained-release preparations available. Clinical features are outlined in Table 28.15.

Table 28.14 Types of calcium channel blockers