history of sympathomimetic poisoning is that the onset of symptoms usually occurs within 2 hours...
TRANSCRIPT
Clinical Presentation
history of sympathomimetic poisoning is that the onset of symptoms usually occurs within 2 hours post exposure
Life-threatening complications typically occur within 2-6 hours postexposure.
duration of action of illegal sympathomimetic agents differ based on their chemical structure. Methamphetamine has the chemical structure of amphetamine with an additional methyl group. The half-life of methamphetamine, however, is much longer (2-24 h) than that of amphetamine
The route of abuse also contributes to the duration of action of some of these illegal sympathomimetic agents.
the half-life of methamphetamine ranges from 10-20 hours, depending on the urine pH, history of recent use, and dosage.[11]
Metabolism occurs faster in acidic urine
The majority of methamphetamine is metabolized to amphetamine, which provides further CNS stimulation.
adverse effects of MDMA are not clearly dose related
some individuals developing life-threatening toxic syndromes after single doses of drug
MDMA-Induced Serotonin Neurotoxicity
Mortality/Morbidity
Acute methamphetamine overdose may result in sympathetic overdrive, cardiovascular collapse, rhabdomyolysis, ventricular tachyarrhythmia, and death.
Injuries from blunt and penetrating
trauma are common
Clinical Presentation
Cardiovascular
Chest pain, aortic dissection, myocardial ischemia/infarction
Palpitations, tachyarrhythmia Dyspnea and edema Hypertension
Central nervous system manifestations
Agitation, violent behavior, self-harm Coma New-onset seizure, movement disorders Emotional lability, confusion, psychosis,
paranoia, hypersexuality, and hallucinations Headache
Headache and cerebrovascular accidents with focal neurologic deficits may be caused by hemorrhage or vasospasm, cerebral edema, and cerebral vasculitis
Coma may result from depletion of catecholamine stores
or concomitant ingestion of sedatives such as ethanol or narcotics
Renal failure
Hypoxemia Rhabdomyolysis Necrotizing angiitis Acute interstitial nephritis Cardiovascular shock with subsequent
acute tubular necrosis
nonlethal signs and symptoms
Mydriasis Tachycardia Diaphoresis Acute psychosis Paranoia Delirium Bruxism (amphetamines and bath salts)
Differential Diagnoses
Acute Coronary Syndrome Acute Respiratory Distress Syndrome Cardiomyopathy, Dilated Hypertensive Emergencies Hyperthyroidism, Thyroid Storm Seizures Subarachnoid Hemorrhage Toxicity, Anticholinergic Toxicity, Antihistamine
Workup
CBC and chemistry test To assess renal and electrolyte function Creatine kinase and/or myoglobin levels To exclude rhabdomyolysis Serial troponin levels - If there is concern for
myocardial ischemia Pregnancy test - In women of childbearing age Toxicology screens - Useful for patients who
cannot or will not disclose drug use history and for pediatric patients with new-onset seizure
ECG for patients with chest pain, altered mental status, and tachycardia.
Procedures
Lumbar puncture may be indicated in patients with altered mental status
to rule out meningitis or subarachnoid hemorrhage.
Imaging Studies
chest radiograph for patients with pulmonary symptoms or chest trauma.
In patients with altered mental status, perform a head CT scan to exclude intracranial bleeding. Such bleeding may be the result of either methamphetamine-induced hypertension or associated head trauma.
Patients who are suspected body-packers, body-stuffers, should undergo abdominal imaging.
sympathomimetic toxicity
because no antidote exists. Assessment of the airway, breathing,
and circulation immediately is recommended.
close monitoring of the vital signs is recommended.
Sedation Protocol
Aim :control dangerous behaviour sufficiently
to facilitate accurate assessment and appropriate management
benzodiazepines are first line treatment agitated patients induced seizures cardiac toxicity
Acute Behavioural Disturbance
primary aim of management is to reduce the risk of harm to the patient, staff and other
people physical restraint alone is often not adequate may actually cause harm if agitation
increases.
Stimulant use risk factor for sudden death of individuals being physically restrained
Sedation Protocol
Oral diazepam 10-20mgs orally. If no clinical response at
30 MIN , an additional 10 mgs this regime until the patient is in a state
of drowsiness or a total dose of 60mgs
Sedation Protocol Intravenous diazepam 2.5-5mg to assess patients Sensitivity to
BZ Some patients will respond to this low dose.
If no clinical response at 10 min an Additional higher dose of 5-10 mg
Repeat this higher dose of 5-10mg every 10 min to a maximum dose of 60mg
if the patient is not sedated adequately. Consider alternate agent Midazolam 5 -10mg IM at 10 min or 2/5-5 IV (to a maximum dose of 25mg)
droperidol 2.5mg intravenously or olanzapine
10mg intramuscular (IM) if no response
Sedation ProtocolORAL DIAZEPAM
INTRAVENOUS DIAZEPAM
10-20mgs orally. If no clinical response at 30 min
, an additional 10 mgs should be administered. this regime until the
patient is in a state of drowsiness or a total
dose of 60mgs
2.5-5mg to assess patients Sensitivity to BZ Some patients will respond to this low dose.
If no clinical response at 10 min an Additional higher dose of 5-10 mg
Repeat this higher dose of 5-10mg every 10 min to a maximum dose of 60mg
if the patient is not sedated adequately. Consider alternate agent droperidol 2.5mg intravenously or
olanzapine 10mg intramuscular (IM) if no response
Observations
Patients should then be monitored for four hours,
Observations should be every 10 minutes for 30 minutes then every 15 minutes for 30 minutes , then every 30 minutes for 60 minutes then hourly for four hours or until awake.
Observations should include:
airway patient colour continuous oxygen saturation respiration rate blood pressure pulse temperature Glasgow Coma Scale score bedside BSL.
Cardiovascular Complications:
uncontrolled hypertension might be at risk for subarachnoid and intracerebral haemorrhage
chest pain benzodiazepines Sublingual nitroglycerine Beta-blockers, should be avoided
Serotonin Toxicity (including Hyperthermia)
Serotonin involved in a range of functions including:
mood, appetite and sleep regulation cognition; perception; motor activity;
temperature regulation; pain control sexual behaviour and hormone secretion
treatment of serotonin toxicity
hyperthermia above 39.5OC intubation with deep intravenous sedation IV fluids/volume resuscitation for dehydration,
hypotension or rhabdomyolysis (ensure adequate urine output
in 1.5-2mls/kg/hr) mechanical ventilation for respiratory
compromise and sedation with IV benzodiazepines might be indicated
treatment of serotonin toxicity
5-HT2 antagonists such as olanzapine (24), chlorpromazine or
cyproheptadine (3) may be indicated (these specific antagonists should
only be used if the diagnosis of serotonin toxicity has been established
and anticholinergic agents have not been co-ingested)
paralysis and intubation may have a role in cases of severe intractable
rigidity management of secondary cardiac arrhythmias or
seizures involves standard measures
measure the core temperature of sympathomimetic poisoned patients.
If hyperthermia is present, standard cooling measures should be initiated.
Controlling agitation significantly helps in cooling a hyperthermic patient.
Hypertension unresponsive to sedation should be treated with a rapidly acting
and easily titrated agent (eg, sodium nitroprusside).
Seizures should be rapidly controlled with benzodiazepines and/or barbiturates.
Obtaining a CT scan of the brain for all sympathomimetic toxic patients who seize, develop a focal neurologic deficit, or experience a severe headache with or without accompanying hypertension is recommended
Prolonged critical care management often is required for the numerous complications that may occur with the severe overdose (eg, hyperthermia, seizures, advanced respiratory distress syndrome [ARDS], renal failure, rhabdomyolysis, CNS dysfunction).
A 19-year-old man was arrested after a traffic violation
and taken to the local jail. he had ingested 8 "balls" (8 g) of
methamphetamine
Personnel at the scene said that the man had had no seizures
but they did witness severe rigors with diaphoresis for approximately 30 minutes
Initially the patient was able to communicate
with difficulty. his last use was at least 10 hours earlier patient as red, cool, and diaphoretic, with severe shakes and incontinent of
urine His lungs were clear, and RR 60/min EKG revealed a sinus tachycardia of
200/min. Pulse oximetry 2.5 Llmin of oxygen was
91 %. blood glucose was 81 mg/dL
On arrival at the emergency department patient's rectal temperature was greater than 108°F,respirations were 45/min, pulse was 180/min , blood pressure was 186/96 mm Hg. Pulse oximetry on 10 Llmin of oxygen was 98% saturated. The patient displayed diffuse rigidity and tremulousness, his skin was hot and
diaphoretic, his pupils were dilated and he did not
respond to verbal or painful stimuli A Foley catheter returned minimal urine
output.
Ice packs on the patient's groin, axillae, and neck
lowered his temperature to 105.5°F. During resuscitation
he received sequential trials of lorazepam, labetalol, and 50% dextrose
in water. His blood pressure decreased to 86/44
mm Hg
After a trial of lidocaine for his tachycardia, the patient's heart rate decreased to 140 beats per minute.
Intravenous normal saline was rapidly infused. His respiratory status worsened, and pulse oximetry dropped to 63 % saturation on 10 Llmin of oxygen. He was intubated orally with difficulty because of
teeth clenching. Gastric lavage produced a string, but there were
no pill fragments. Sorbitol and activated charcoal were
administered, and the patient was given intravenous famotidine. rectal examination showed no pill fragments or other foreign bodies.
A chest radiograph CT scan of the head were negative
An electrocardiogram continued to show sinus tachycardia..
Initial chemistry and coagulation laboratory values were all essentially normal
Arterial blood gases indicated metabolic acidosis.
The patient was transferred to the critical care unit 3 hours after his arrest by police, when it is presumed that he had swallowed the
8 "balls" to avoid detection . A drug-screening test of blood drawn 8 hours
after admission was negative for alcohol. Cannabinoids were present. His blood was positive for amphetamines, with a serum value
of 3,500 ng/mL (3.5 mglL).
patient's liver function tests continued to worsen from day 2, with enzyme levels reaching their highest on day 4 at an AST level of 4,422
UIL and alanine aminotransferase (ALT) of2,786 UIL. The transaminase levels subsequently decreased rapidly with a delayed increase in total bilirubin. Serum creatine kinase levels exceeded 20,000
UIL on day 2
Dialysis was begun on day 4. His neurologic status never improved
during hospitalization Multiple cardiac arrests occurred
Management of amphetamine toxicity
start with the ARCs (airway, breathing, and circulation)
when apnea, cardiac arrest, dysrhythmias, or
seizures are the initial signs
Although urinary acidification can increase the elimination of amphetamines, is no recommended because of the
possibility of worsening renal insult from rhabdomyolysis. better to promote urine output with rapid, generous intravenous fluid
resuscitation to maintain an alkaline urine to alleviate
the effects of myoglobin on the kidneys
It is important to recognise that psychostimulant toxicity can occur among
both experimental and regular users of psychostimulants
If the Patient is Cooperative
type of psychostimulant used amount of psychostimulant used1 time of administration route of administration (intranasal, intravenous, oral, inhalation) frequency of use (e.g. regular daily use, binge pattern, recreational, experimental, etc) duration of current use and age of first use obtain a urine sample for a drug screen if possible. 2. Other drug use concurrent use of other drugs (particularly alcohol, benzodiazepines, opiates, party drugs), including criteria above concurrent use of antidepressant medication (e.g. TCAs, MAOIs, SSRIs, bupropion, venlaxafine) which may increase the serotonergic or catecholamine mediated effects of psychostimulants
If the Patient is not Cooperative
signs might indicate the patient has recently used
dilated pupils that react sluggishly to light clenched jaw or muscle rigidity restlessness, agitation, tremor or repetitive
movements rapid speech motor agitation or pacing hypertension tachycardia sweaty palms, flushed diaphoretic facial skin hypervigilance, paranoia.
Dantrolene was prescribed for temperatures of 104°F and higher.
Temperature decreased to 103.6°F with cooling measures and the paralytic. He remained comatose with a Glasgow score of 3 He began to ooze blood from various orifices His fibrinogen decreased from 128 mg/dL to 85 during the first 14 hours. His BUN and CR levels elevated on day 2 of
hospitalization. His AST level was elevated to 1,927 urine became positive for myoglobin