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Acute poisonings and comatous state
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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. Classification of consciousness levels according to Bogolepow, 1982. Conscious (normal) Confused Stuporous Soporous Comatose: moderate deep terminal Each level has its own diagnostic criteria; you can find them in the table below.
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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.).
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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: Cheyne- Stokes 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.
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Identification of intoxication Suspition of intoxication Vilnius toxikology clinic 2003 Preliminary CNS evaluation SuppressionAgitation Opioids THC EthanolPsichostimulants Midriasis, normal photoreaction Normal pupils, photoreactionMyosis, no photoreaction
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Opioids Natural (opiates) Morphine Codeine Semisynthetic Heroin Hydromorphone Oxymorphone Oxycodone Synthetic Methadone Meperidine Levorphal Fentanyl 3-methylfentanyl Propoxyphene Tramadol
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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
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Opioid overdose CNS Symptoms I Respiratory depression, intensive central cyanosis (bradipnoe 2-4/min.) Sedation and drowsiness, unconsciousness up to coma Miosis Hypothermia
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Opioid overdose CNS Symptoms II Suppression of cough Suppression of pain Nausea and vomiting Euphoria or dysphoria Seizures
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Opioid overdose Periphery Symptoms Cardiovascular: vasodilatation, hypotension Urinary tract: urinary urgency and retention Skin: urticaria from histamine release GI tract: constipation Uterus: decreased contractions
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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
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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
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Cocaine Neurotransmission I http://drugabuse.gov
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Cocaine Neurotransmission II http://drugabuse.gov
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Cocaine Neurotransmission III http://drugabuse.gov
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Cocaine overdose Symptoms I Agitation to psychosis Halucinations Mydriasis Hypertermia (>41 O C) Hypertension Tachycardia Seizures Coma
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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 fibrilation
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Cocaine overdose Treatment No antidotes CPR Agitation, psychosis, seizures, hypertension, tachycardia BZD (Diazepam 10-100 mg) Hyperthermia external cooling (<41 O C) Severe hypertension phentolamin, nitropruside SVT - Ca antagonists VT - lidocaine No β-blockers
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Heroin+Cocaine overdose Symptoms Changing clinical signs (swing) Cocaine ↔ opioids Coma Respiratory depression Midriasis Tachycardia
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Heroin+Cocaine overdose Treatment CPR Naloxone: bolus 2 mg i/v + continous infusion In-patient monitoring at least 12 hours Symptomic treatment Benzodiazepines
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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
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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
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Body packing and stuffing Investigations StudyIndicationsSensivityComments 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 Radiographic Approaches to the Identification of Body packing
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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)
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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
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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
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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
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Body packing and stuffing First detected case in Lithuania “double condom’’ sign Fill defects
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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
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Body packing and stuffing First detected case in Lithuania 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” Forensic analysis
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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 body- packing Surgery is indicated for patients with acute cocaine poisoning or gastrointestinal obstruction or perforation Observation till the last package removes is obligatory
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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
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Amphetamine Symptoms 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
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“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 “Exploding chest” Sedation Ataxia Tremor Dry mouth Tachycardia Injected conjunctive
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Cannabinoids Treatment Benzodiazepines Symptomic treatment Psychoterapy
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LSD Symptoms Anxiety, agitation Hallucinations Moist and pale skin Mild hypertension Tachycardia Hypertermia (Lysergic Acid Diethylamine)
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LSD Treatment Benzodiazepines In severe cases – the same as amphetamines (Lysergic Acid Diethylamine)
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Gamma-hydroxybutyric acid Symptoms CNS depression (GCS of 3 is not uncommon) (GCS of 3 is not uncommon) Extreme combativeness and agitation Bradycardia Decreased systemic vascular resistance, hypotension Profound respiratory depression.
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Gamma-hydroxybutyric acid Treatment Airway protection and aspiration precautions Use atropine to treat symptomatic bradycardia that is unresponsive to stimulation
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Solvents Symptoms Agitation, joy Vertigo, coordination damamge Sneeze, hypersalivation CNS depression, delusions Sense of invulnerability Respiratory depression Tachycardia Seizures, coma
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Solvents Treatment Oxygen CPR (if needed) Benzodiazepines Symptomic treatment
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Milestones in treatment of drug overdose NaloxoneBenzodiazepines Life support measures
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