Transcript Acute poisonings with substance of abuse

Acute poisonings and
comatous state
Classification, clinic and diagnostics
of coma
 Classification, clinic and diagnostics of coma.
 Coma is a complete depression of consciousness with lack of pain
sensitivity and reflexes, general muscular relaxation and violated vital
functions.
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 Classification of consciousness levels according to Bogolepow, 1982.
 Conscious (normal)
 Confused
 Stuporous
 Soporous
 Comatose: moderate
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deep
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terminal
 Each level has its own diagnostic criteria; you can find them in the table
below.
 Classification of coma according to etiology and pathogenesis.
 Coma of central genesis (epileptic, traumatic, apoplectic).
 Coma caused by visceral organs dysfunctions and endocrine glands
disorders (diabetic, hypoglycaemic, thyrotoxic, myxedemic,
hypopituitary, hypocorticoid, hepatic, uremic, hypochloremic, anaemic,
alimentary-distrophic ).
 Infectious coma (in case of pneumonia, malaria, neuronal infections,
etc.).
 Acute toxic coma (poisonings with alcohol and its surrogates, medicinal
poisonings, carbon monoxide poisonings).
 Coma caused by physical factors ( caused by electric injury,
hypothermic and hyperthermia coma, radiation coma, etc.).
 Sometimes it is very hard to find the reason of the coma, so detailed
anamnesis (interview relatives and witnesses) and clinical observations
are very important.
 First of all ask about the duration of unconsciousness and was it lost
suddenly or there were other levels of altered consciousness. Ask
about the events prior to incident: did the patient fell and was there a
chance of head injury? Did he have fever, flu or jaundice? Are there
any sings of chronic diseases like diabetes, epilepsy, hypertonic
disease? Have the patient ever suffered from similar unconsciousness
episodes? Were there any suicide attempts? If the comatose condition
was not sudden, have the patient complained of vomiting, convulsions?
Pay attention to the personal things of the patient: you can find medical
documents, medicine packages, diabetic bracelets or necklaces, etc.
 If the anamnesis failed to reveal the coma etiology, concentrate on
objective symptoms.
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Skin colour: extreme paleness can be a sign of great blood loss, circulatory
collapse, blood diseases. Cyanosis is a symptom of hypercapnic coma caused
by respiratory failure or asphyxia (hanging, drowning, convulsions).
Hyperaemic face allows you to think about atropine and carbon monoxide
poisonings, hyperglycaemic coma or infectious disease.
Head position: tilted back head is a sign of meningitis, tetanus, hysteria; head
turned aside can be the symptom of stroke.
Pathological types of breathing are also helpful in coma diagnostics: CheyneStokes breathing (periods of apnoea, which are followed with chaotic frequent
breathing) and Biot’s breathing (periods of apnoea which are followed with
breathing of equal amplitude) show deep affection of central nervous system.
Kussmaul breathing (deep and laboured) proves accumulation of acid
metabolites (metabolic acidosis) of exogenous (in case of poisonings) or
endogenous (diabetic ketoacidosis) nature. Fever and rapid deep breathing are
probable signs of infectious coma. Remember that per each excess body
temperature degree there are 5-7 excess breathes and 10 excess heart beats.
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Generally when you are coming to the patient with consciousness disorders try
to do this from the side of patient’s head (nape): this way you can easily
improve airways patency if necessary (thrust the jaw forward for example) and
avoid accidental injuries from the patient if his moves are uncontrolled.
You can always identify simulation or hysteric coma by opening the eyes of the
patient: in case of simulating conscious patients or hysteric patients you will
feel the resistance of the eyelids. Unconscious patients never resist when you
try to open their eyes.
Pressing the eyeballs toy can evaluate their tone: “soft” eyeballs with
decreased tone are the symptom of hypovolemia (bleeding, dehydration) or
shock condition. However they can also be part of hyperglycaemic coma clinic.
The depth of coma is assessed with the reflexes reduction. If patient reacts to
the external stimuli - it’s a moderate coma. If corneal reflexes are preserved
with depressed other reflexes – it’s a deep coma. Lack of photoreaction is a
symptom of terminal coma.
Identification of intoxication
Suspition of intoxication
Preliminary CNS evaluation
Agitation
Midriasis, normal photoreaction
Psichostimulants
Suppression
Normal pupils, photoreaction
Ethanol
Myosis, no photoreaction
Opioids
THC
Vilnius toxikology clinic 2003
Opioids
Natural
(opiates)
Morphine
Codeine
Semisynthetic
Heroin
Hydromorphone
Oxymorphone
Oxycodone
Synthetic
Methadone
Meperidine
Levorphal
Fentanyl
3-methylfentanyl
Propoxyphene
Tramadol
Opioids
Pharmacology
Generally, all opioid agonist drugs exert
the same pharmacological effects in
the CNS and periphery, but differ in
pharmacokinetic properties, e.g.
duration of action, potency, ability to
cross blood-brain-barrier
Opioid overdose
CNS Symptoms I
 Respiratory depression, intensive central
cyanosis (bradipnoe 2-4/min.)
 Sedation and drowsiness, unconsciousness
up to coma
 Miosis
 Hypothermia
Opioid overdose
CNS Symptoms II
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Suppression of cough
Suppression of pain
Nausea and vomiting
Euphoria or dysphoria
Seizures
Opioid overdose
Periphery Symptoms
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Cardiovascular: vasodilatation, hypotension
Urinary tract: urinary urgency and retention
Skin: urticaria from histamine release
GI tract: constipation
Uterus: decreased contractions
Opioid overdose
Treatment
 CPR (cardiopulmonary resuscitation)
 Naloxone – bolus 2 mg I/V (0,4-2mg) to
10 mg (If no I/V access - sublingual,
endotracheal, i/m), continous infusion
 In-patient monitoring at least 12 hours
 Heating
Cocaine
Neurochemical actions
 Blockade of reuptake of NE, DA and
serotonin:
– Low dose: preferential action on NE reuptake
– Moderate dose: NE and DA reuptake
– High doses: NE, DA and serotonin reuptake
 Local anesthetic action:
– blockade of sodium channels
Cocaine
Neurotransmission I
http://drugabuse.gov
Cocaine
Neurotransmission II
http://drugabuse.gov
Cocaine
Neurotransmission III
http://drugabuse.gov
Cocaine overdose
Symptoms I
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Agitation to psychosis
Halucinations
Mydriasis
Hypertermia (>41OC)
Hypertension
Tachycardia
Seizures
Coma
Cocaine overdose
Symptoms II
 Ischemic complications (vasospasm)
– Myocardial infarction, cerebral infarction, etc.
 Haemorrhagic complications
(hypertension)
– Subarachnoid, intracerebral hemorrhage,
aortic dissection, etc.
 Dysrhytmias to ventricular
fibrilation
Cocaine overdose
Treatment
No antidotes
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 CPR
 Agitation, psychosis, seizures, hypertension,
tachycardia BZD (Diazepam 10-100 mg)
 Hyperthermia external cooling (<41OC)
 Severe hypertension phentolamin, nitropruside
 SVT - Ca antagonists
 VT - lidocaine
 No β-blockers
Heroin+Cocaine overdose
Symptoms
 Changing clinical signs (swing)
Cocaine ↔ opioids
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Coma
Respiratory depression
Midriasis
Tachycardia
Heroin+Cocaine overdose
Treatment
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CPR
Naloxone: bolus 2 mg i/v + continous infusion
In-patient monitoring at least 12 hours
Symptomic treatment
Benzodiazepines
Body packing and stuffing
Is it the same?
 Packing – action,
when a person
transports illicit drugs
in a body orifice. The
risk of package rupture
is more remote.
 Stuffing – action, when a
person places drugs in a
body orifice in a moment
of imminent danger. In
this case drugs are not
well packaged for
transportation, hence the
high risk for leakage
Body packing and stuffing
Investigations
 Ultrasonography
 Contrast X-ray of
the bowel
 Computerized
tomography
 Drug detection in
urine and blood
 Clinical observation
 Light solid diet
 Free assumption of
liquids
 Surgical removal, if
mechanical obstruction
occurs
 Treatment of systemic
symptoms
Body packing and stuffing
Investigations
Radiographic Approaches to the Identification of Body packing
Study
Indications
Sensivity
Comments
Plain
abdominal
radiography
Screening test
85-90%
Sensivity for finding small
numbers of packets may be
lower. May miss substantial
numbers of packets
Ultrasonogra
phy
Screening test
No
established
Has the potential to be very
useful, large studies needed
CT
Used if equivocal results
obtained on initial screening
test. Used to document that
GT is clear
No
established
Large studies needed
Contrast
enhanced
abdominal
radiography
Used if equivocal results
obtained on initial screening
test. Used to document that
GT is clear
96%
Reported sensitivity based
on 1 study
Body packing and stuffing
Levels of packages security
 I - 1 protective layer
 II - 2 protective layers;
in our case
 III – machine-made (4-7
protective layers)
Body packing and stuffing
First detected case in Lithuania
 A 31 year old male was brought to the
Department of Toxicology by customs
officers after disembarking at the Vilnius
International Airport suspecting of cocaine
transport
Body packing and stuffing
First detected case in Lithuania
 There were no any complaints and examination
of patient didn’t show any pathology
 All blood tests were normal
 Patient refused endoscopy, but agree to
contrast X- ray investigation
 Foreign bodies were detected in the
gastrointestinal tract by X-ray photography
 Toxicological analysis for narcotics of urine and
blood were done
Body packing and stuffing
First detected case in Lithuania
 Observation (blood pressure, heart
frequency, temperature, neurological
assessment every hour)
 Mild laxative in conjunction with sufficient
beverages
Body packing and stuffing
First detected case in Lithuania
Fill defects
“double condom’’ sign
Body packing and stuffing
First detected case in Lithuania
39 packets were excreted on the first day, 10 – on
the second day, 3 – at the third day
X-ray 3 days later revealed foreign bodies in the
gastrointestinal tract (“double condom’’ sign)
Because of customs officers demand the patient was
transferred to the Hospital of Prison, despite staff
objection. 62 cocaine packets were excreted
during the next 3 days
Body packing and stuffing
First detected case in Lithuania
Forensic analysis
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Condoms were filled with 3-8 g of cocaine each
114 packages, weight 438,63 g,purity – 57%
2 of cocaine packets were slightly injured
Blood sample – no answer, urine analysis –
“possibility of cocaine metabolites”
Body packing and stuffing
Management
•In no way endoscopic removal of the package should be
attempted. The patient in whom only one packet fails to
pass the pylorus may be the exception
•Conservative management during spontaneous evacuation
of the containers is the first choice approach to the bodypacking
•Surgery is indicated for patients with acute cocaine
poisoning or gastrointestinal obstruction or perforation
•Observation till the last package removes is obligatory
Amphetamine
Neurochemical actions
 Dose-related increase in release of
norepinephrine, dopamine and serotonin:
– low dose: preferential action on NE release
– moderate dose: NE and DA release
– high dose: NE, DA and serotonin release
 Blockade of reuptake of NE, DA and serotonin
 Inhibition of MAO
Amphetamine
Symptoms
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Agitation to psychosis
Halucinations
Mydriasis
Tachycardia
Hypertension
Mild hypertermia
Seizures
Coma
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Amphetamine
Treatment
No antidotes
CPR
GI decontamination gastric lavage, activated charcoal
Benzodiazepines
Severe hypertension phentolamin, nitropruside
External cooling
SVT Ca antagonists
VT lidocaine
 No β-blockers
“Ecstasy” (MDMA):
a hallucinogenic amphetamine
 Combination of psychostimulant effects with
stronger hallucinogenic effects (serotonin
component)
 Common acute adverse effects: muscle
tension and bruxism
 Hyperthermia
 Increase HR and BP
 Acne-like rash
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Cannabinoids
Symptoms
Impairment of cognitive function
Disorientation, talkativness
Anxiety to panic
Headache
 Ataxia
“Exploding chest”
 Tremor
Sedation
 Dry mouth
 Tachycardia
 Injected
conjunctive
Cannabinoids
Treatment
 Benzodiazepines
 Symptomic treatment
 Psychoterapy
LSD
Symptoms
(Lysergic Acid Diethylamine)
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Anxiety, agitation
Hallucinations
Moist and pale skin
Mild hypertension
Tachycardia
Hypertermia
LSD
Treatment
(Lysergic Acid Diethylamine)
 Benzodiazepines
 In severe cases – the same as
amphetamines
Gamma-hydroxybutyric acid
Symptoms
 CNS depression
(GCS of 3 is not uncommon)
 Extreme combativeness and
agitation
 Bradycardia
 Decreased systemic vascular
resistance, hypotension
 Profound respiratory depression.
Gamma-hydroxybutyric acid
Treatment
 Airway protection and
aspiration precautions
 Use atropine to treat
symptomatic bradycardia that
is unresponsive to stimulation
Solvents
Symptoms
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Agitation, joy
Vertigo, coordination damamge
Sneeze, hypersalivation
CNS depression, delusions
Sense of invulnerability
Respiratory depression
Tachycardia
Seizures, coma
Solvents
Treatment
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Oxygen
CPR (if needed)
Benzodiazepines
Symptomic treatment
Milestones in treatment of
drug overdose
Naloxone
Benzodiazepines
Life support measures