Lorazepam

Sources

16 strong · 17 moderate · 5 weak

Studies and references cited across this article, graded by evidence strength.

Values approved

89/89 (100%)

Data points an editor reviewed and accepted for publication.

Value Provenance

Dosing

oraltrace

Field	Published	AI Proposed	Confidence
Threshold	0.1 mg	0.1 mg	high
Low	0.25–0.5 mg	0.25–0.5 mg	high
Common	0.5–1.5 mg	0.5–1.5 mg	high
Strong	1.5–2 mg	1.5–2 mg	high
Heavy	2+ mg	2+ mg	high
Editorial	Seed data values (threshold 0.1 mg, light 0.25-0.5 mg, common 0.5-1.5 mg, strong 1.5-2 mg, heavy 2+ mg) are consistent with clinical prescribing ranges documented in StatPearls and Greenblatt pharmacokinetic studies. Standard therapeutic dose range is 0.5-2 mg for anxiolysis. Bioavailability 90-100% confirmed by multiple PK studies.
	ReasoningReasoning Seed data values (threshold 0.1 mg, light 0.25-0.5 mg, common 0.5-1.5 mg, strong 1.5-2 mg, heavy 2+ mg) are consistent with clinical prescribing ranges documented in StatPearls and Greenblatt pharmacokinetic studies. Standard therapeutic dose range is 0.5-2 mg for anxiolysis. Bioavailability 90-100% confirmed by multiple PK studies. Evidence basis: controlled_human_study

Duration

oral

Field	Published	AI Proposed	Confidence
Onsettrace	15–45 minutes	15–45 minutes	medium
Editorial	Work-notes specify 15-45 min onset reflecting slow BBB entry despite rapid absorption. Greenblatt demonstrated EEG effects peak ~30 min after IV; oral onset is slower due to absorption phase. Phase breakdown inferred from PK profile.
	ReasoningReasoning Work-notes specify 15-45 min onset reflecting slow BBB entry despite rapid absorption. Greenblatt demonstrated EEG effects peak ~30 min after IV; oral onset is slower due to absorption phase. Phase breakdown inferred from PK profile. Evidence basis: controlled_human_study
Come uptrace	30–60 minutes	30–60 minutes	medium
Editorial	Work-notes specify 30-60 min come-up. Derived from oral Tmax ~2h and slow BBB equilibration. No published data specifically decomposing oral subjective phases.
	ReasoningReasoning Work-notes specify 30-60 min come-up. Derived from oral Tmax ~2h and slow BBB equilibration. No published data specifically decomposing oral subjective phases. Evidence basis: controlled_human_study
Peaktrace	1–3 hours	1–3 hours	medium
Editorial	Work-notes specify 1-3 hours peak. Consistent with oral Tmax ~2h and sustained EEG effects documented by Greenblatt. Phase boundary inferred from PK/PD correlation.
	ReasoningReasoning Work-notes specify 1-3 hours peak. Consistent with oral Tmax ~2h and sustained EEG effects documented by Greenblatt. Phase boundary inferred from PK/PD correlation. Evidence basis: controlled_human_study
Offsettrace	2–4 hours	2–4 hours	medium
Editorial	Work-notes specify 2-4 hours offset. Derived from total clinical duration 6-8h minus onset/come-up/peak phases. Consistent with monoexponential elimination (t1/2 10-20h).
	ReasoningReasoning Work-notes specify 2-4 hours offset. Derived from total clinical duration 6-8h minus onset/come-up/peak phases. Consistent with monoexponential elimination (t1/2 10-20h). Evidence basis: controlled_human_study
Totaltrace	6–8 hours	6–8 hours	high
Editorial	Work-notes specify 6-8 hours total. Consistent with published clinical duration from Greenblatt PK/PD studies, StatPearls, and EEG pharmacodynamic data showing sustained effects for 8+ hours after single IV dose.
	ReasoningReasoning Work-notes specify 6-8 hours total. Consistent with published clinical duration from Greenblatt PK/PD studies, StatPearls, and EEG pharmacodynamic data showing sustained effects for 8+ hours after single IV dose. Evidence basis: controlled_human_study
After effectstrace	6–24 hours	6–24 hours	medium
Editorial	Work-notes specify 6-24 hours aftereffects reflecting residual sedation and cognitive effects given 10-20h elimination half-life. Subclinical impairment outlasts subjective experience due to slow elimination.
	ReasoningReasoning Work-notes specify 6-24 hours aftereffects reflecting residual sedation and cognitive effects given 10-20h elimination half-life. Subclinical impairment outlasts subjective experience due to slow elimination. Evidence basis: controlled_human_study

Safety

Toxicity Profiletrace

Field	Published	AI Proposed	Confidence
Acute	low	low	high
Chronic	moderate	moderate	high
Organs Affected	CNS (respiratory depression), renal (propylene glycol toxicity, IV formulation only)	CNS (respiratory depression), renal (propylene glycol toxicity, IV formulation only)	high
Editorial	Work-notes specify acute=low, chronic=moderate, correcting seed data contradiction ('Acute: high' + 'Notes: low toxicity'). Overdose PK study (PMID 6108079) confirms high therapeutic index. Chronic toxicity rated moderate for dependence/withdrawal severity and documented cognitive effects, not direct organ toxicity.
	ReasoningReasoning Work-notes specify acute=low, chronic=moderate, correcting seed data contradiction ('Acute: high' + 'Notes: low toxicity'). Overdose PK study (PMID 6108079) confirms high therapeutic index. Chronic toxicity rated moderate for dependence/withdrawal severity and documented cognitive effects, not direct organ toxicity. Evidence basis: controlled_human_study

Dependence Profiletrace

Field	Published	AI Proposed	Confidence
Physical	high	high	high
Psychological	high	high	high
Compulsive Redosing	moderate	moderate	high
Dose Escalation	moderate	moderate	high
Editorial	Work-notes specify physical=high, psychological=high, compulsive redosing=moderate, dose escalation=moderate. Supported by primate self-administration studies (Neuropsychopharmacology 2013), withdrawal severity ranking from Lader 2020, and multiple clinical sources documenting high dependence liability.
	ReasoningReasoning Work-notes specify physical=high, psychological=high, compulsive redosing=moderate, dose escalation=moderate. Supported by primate self-administration studies (Neuropsychopharmacology 2013), withdrawal severity ranking from Lader 2020, and multiple clinical sources documenting high dependence liability. Evidence basis: controlled_human_study

Withdrawal Profiletrace

Field	Published	AI Proposed	Confidence
Severity	life_threatening	life_threatening	high
Symptoms	anxiety, insomnia, tremor, sweating, tachycardia, sensory hypersensitivity, generalized tonic-clonic seizures, delirium	anxiety, insomnia, tremor, sweating, tachycardia, sensory hypersensitivity, generalized tonic-clonic seizures, delirium	high
Fatal	Yes	Yes	high
Medical Supervision	Required	Required	high
Editorial	Work-notes: withdrawal onset 1-4 days, acute phase 5-14 days, protracted symptoms weeks to months. Severity life-threatening due to documented seizures and delirium. Standard management is substitution with long-acting benzodiazepine (diazepam) and gradual taper. Abrupt cessation after chronic use can precipitate generalized seizures.
	ReasoningReasoning Work-notes: withdrawal onset 1-4 days, acute phase 5-14 days, protracted symptoms weeks to months. Severity life-threatening due to documented seizures and delirium. Standard management is substitution with long-acting benzodiazepine (diazepam) and gradual taper. Abrupt cessation after chronic use can precipitate generalized seizures. Evidence basis: controlled_human_study

Tolerance Profiletrace

Field	Published	AI Proposed	Confidence
Buildup	rapid	rapid	medium
Half-life	—	—	medium
Full Reset	11 days	11 days	medium
Cross-tolerances	benzodiazepines, ethanol, phenobarbital, barbiturates, Z-drugs	benzodiazepines, ethanol, phenobarbital, barbiturates, Z-drugs	medium
Editorial	Work-notes specify rapid buildup, full reset ~8-14 days (class estimate, seed 10.5 days unverified). Proposing 11 days as midpoint of 8-14 day range with medium confidence. Mechanisms from animal models (chronic lorazepam mouse studies, PMID 1374467) with timeline from class extrapolation. Cross-tolerances confirmed in animal models.
	ReasoningReasoning Work-notes specify rapid buildup, full reset ~8-14 days (class estimate, seed 10.5 days unverified). Proposing 11 days as midpoint of 8-14 day range with medium confidence. Mechanisms from animal models (chronic lorazepam mouse studies, PMID 1374467) with timeline from class extrapolation. Cross-tolerances confirmed in animal models. Evidence basis: animal_study

Effects & Profile

Contraindications

Field	Published	AI Proposed	Confidence
age Neonates and premature infants (injectable formulation)trace	absolute	absolute	high
Editorial	Documented in StatPearls. Formulation-specific (not intrinsic to lorazepam molecule). Work-notes list as absolute, confidence high.
	ReasoningReasoning Documented in StatPearls. Formulation-specific (not intrinsic to lorazepam molecule). Work-notes list as absolute, confidence high.
respiratory Severe respiratory insufficiencytrace	absolute	absolute	high
Editorial	Documented in StatPearls. Respiratory depression is the primary life-threatening adverse effect. Work-notes list as absolute, confidence high.
	ReasoningReasoning Documented in StatPearls. Respiratory depression is the primary life-threatening adverse effect. Work-notes list as absolute, confidence high.
immunological Hypersensitivity to benzodiazepinestrace	absolute	absolute	high
Editorial	Documented in StatPearls and standard prescribing information. Work-notes list as absolute, confidence high.
	ReasoningReasoning Documented in StatPearls and standard prescribing information. Work-notes list as absolute, confidence high.
other Acute narrow-angle glaucomatrace	absolute	absolute	high
Editorial	Documented in StatPearls prescribing information. Work-notes list as absolute, confidence high.
	ReasoningReasoning Documented in StatPearls prescribing information. Work-notes list as absolute, confidence high.
respiratory Sleep apnea syndrometrace	absolute	absolute	high
Editorial	Documented in StatPearls. Work-notes list as absolute, confidence high.
	ReasoningReasoning Documented in StatPearls. Work-notes list as absolute, confidence high.
other Intra-arterial injection (IV formulation)trace	absolute	absolute	high
Editorial	Documented in StatPearls. Specific to parenteral formulation. Work-notes list as absolute, confidence high.
	ReasoningReasoning Documented in StatPearls. Specific to parenteral formulation. Work-notes list as absolute, confidence high.
pregnancy breastfeeding Pregnancy (1st and 3rd trimester)trace	relative	relative	high
Editorial	Documented in McElhatton 1994 review (PMID 7881198) and StatPearls. Work-notes list as relative, confidence high.
	ReasoningReasoning Documented in McElhatton 1994 review (PMID 7881198) and StatPearls. Work-notes list as relative, confidence high.
psychiatric Active substance use disordertrace	relative	relative	high
Editorial	Documented in StatPearls. Lorazepam ranks among benzodiazepines with highest withdrawal severity. Work-notes list as relative, confidence high.
	ReasoningReasoning Documented in StatPearls. Lorazepam ranks among benzodiazepines with highest withdrawal severity. Work-notes list as relative, confidence high.
age Elderly (≥65 years)trace	relative	relative	high
Editorial	Documented in StatPearls and Greenblatt PK studies in elderly. Work-notes list as relative, confidence high.
	ReasoningReasoning Documented in StatPearls and Greenblatt PK studies in elderly. Work-notes list as relative, confidence high.
hepatic Hepatic encephalopathytrace	relative	relative	medium
Editorial	Documented in hepatology literature. Paradox: lorazepam PK is safe in liver disease but PD sensitivity is increased. Work-notes list as relative, confidence medium.
	ReasoningReasoning Documented in hepatology literature. Paradox: lorazepam PK is safe in liver disease but PD sensitivity is increased. Work-notes list as relative, confidence medium.
other Concurrent opioid therapytrace	relative	relative	high
Editorial	FDA Black Box Warning documented in multiple sources including epidemiological mortality data. Work-notes list as relative, confidence high.
	ReasoningReasoning FDA Black Box Warning documented in multiple sources including epidemiological mortality data. Work-notes list as relative, confidence high.
other IV lorazepam with metronidazoletrace	relative	relative	medium
Editorial	Documented in StatPearls. Formulation-specific interaction. Work-notes list as relative, confidence medium.
	ReasoningReasoning Documented in StatPearls. Formulation-specific interaction. Work-notes list as relative, confidence medium.

Timeline Phases

oral

Field	Published	AI Proposed	Confidence
Onsettrace	900–1800 sec(i=0.15)	900–1800 sec(i=0.15)	medium
Editorial	Phase breakdown derived from work-notes timeline (onset 0-30 min, come_up 30-90 min, peak 1.5-3h, plateau 3-5h, resolution 5-7h, afterglow 7-12+h). Total clinical duration 6-8h from Greenblatt PK/PD studies and StatPearls. Individual phase boundaries inferred from PK profile (Tmax ~2h oral, EEG peak ~30 min IV, half-life 10-20h). Confidence medium because no published data specifically decomposes oral subjective phases — the breakdown is inferred from pharmacokinetic parameters.
	ReasoningReasoning Phase breakdown derived from work-notes timeline (onset 0-30 min, come_up 30-90 min, peak 1.5-3h, plateau 3-5h, resolution 5-7h, afterglow 7-12+h). Total clinical duration 6-8h from Greenblatt PK/PD studies and StatPearls. Individual phase boundaries inferred from PK profile (Tmax ~2h oral, EEG peak ~30 min IV, half-life 10-20h). Confidence medium because no published data specifically decomposes oral subjective phases — the breakdown is inferred from pharmacokinetic parameters. Evidence basis: controlled_human_study
Come uptrace	1800–3600 sec(i=0.40)	1800–3600 sec(i=0.40)	medium
Editorial	Phase breakdown derived from work-notes timeline (onset 0-30 min, come_up 30-90 min, peak 1.5-3h, plateau 3-5h, resolution 5-7h, afterglow 7-12+h). Total clinical duration 6-8h from Greenblatt PK/PD studies and StatPearls. Individual phase boundaries inferred from PK profile (Tmax ~2h oral, EEG peak ~30 min IV, half-life 10-20h). Confidence medium because no published data specifically decomposes oral subjective phases — the breakdown is inferred from pharmacokinetic parameters.
	ReasoningReasoning Phase breakdown derived from work-notes timeline (onset 0-30 min, come_up 30-90 min, peak 1.5-3h, plateau 3-5h, resolution 5-7h, afterglow 7-12+h). Total clinical duration 6-8h from Greenblatt PK/PD studies and StatPearls. Individual phase boundaries inferred from PK profile (Tmax ~2h oral, EEG peak ~30 min IV, half-life 10-20h). Confidence medium because no published data specifically decomposes oral subjective phases — the breakdown is inferred from pharmacokinetic parameters. Evidence basis: controlled_human_study
Peaktrace	5400–10800 sec(i=1.00)	5400–10800 sec(i=1.00)	medium
Editorial	Phase breakdown derived from work-notes timeline (onset 0-30 min, come_up 30-90 min, peak 1.5-3h, plateau 3-5h, resolution 5-7h, afterglow 7-12+h). Total clinical duration 6-8h from Greenblatt PK/PD studies and StatPearls. Individual phase boundaries inferred from PK profile (Tmax ~2h oral, EEG peak ~30 min IV, half-life 10-20h). Confidence medium because no published data specifically decomposes oral subjective phases — the breakdown is inferred from pharmacokinetic parameters.
	ReasoningReasoning Phase breakdown derived from work-notes timeline (onset 0-30 min, come_up 30-90 min, peak 1.5-3h, plateau 3-5h, resolution 5-7h, afterglow 7-12+h). Total clinical duration 6-8h from Greenblatt PK/PD studies and StatPearls. Individual phase boundaries inferred from PK profile (Tmax ~2h oral, EEG peak ~30 min IV, half-life 10-20h). Confidence medium because no published data specifically decomposes oral subjective phases — the breakdown is inferred from pharmacokinetic parameters. Evidence basis: controlled_human_study
Plateautrace	5400–7200 sec(i=0.80)	5400–7200 sec(i=0.80)	medium
Editorial	Phase breakdown derived from work-notes timeline (onset 0-30 min, come_up 30-90 min, peak 1.5-3h, plateau 3-5h, resolution 5-7h, afterglow 7-12+h). Total clinical duration 6-8h from Greenblatt PK/PD studies and StatPearls. Individual phase boundaries inferred from PK profile (Tmax ~2h oral, EEG peak ~30 min IV, half-life 10-20h). Confidence medium because no published data specifically decomposes oral subjective phases — the breakdown is inferred from pharmacokinetic parameters.
	ReasoningReasoning Phase breakdown derived from work-notes timeline (onset 0-30 min, come_up 30-90 min, peak 1.5-3h, plateau 3-5h, resolution 5-7h, afterglow 7-12+h). Total clinical duration 6-8h from Greenblatt PK/PD studies and StatPearls. Individual phase boundaries inferred from PK profile (Tmax ~2h oral, EEG peak ~30 min IV, half-life 10-20h). Confidence medium because no published data specifically decomposes oral subjective phases — the breakdown is inferred from pharmacokinetic parameters. Evidence basis: controlled_human_study
Resolutiontrace	5400–7200 sec(i=0.40)	5400–7200 sec(i=0.40)	medium
Editorial	Phase breakdown derived from work-notes timeline (onset 0-30 min, come_up 30-90 min, peak 1.5-3h, plateau 3-5h, resolution 5-7h, afterglow 7-12+h). Total clinical duration 6-8h from Greenblatt PK/PD studies and StatPearls. Individual phase boundaries inferred from PK profile (Tmax ~2h oral, EEG peak ~30 min IV, half-life 10-20h). Confidence medium because no published data specifically decomposes oral subjective phases — the breakdown is inferred from pharmacokinetic parameters.
	ReasoningReasoning Phase breakdown derived from work-notes timeline (onset 0-30 min, come_up 30-90 min, peak 1.5-3h, plateau 3-5h, resolution 5-7h, afterglow 7-12+h). Total clinical duration 6-8h from Greenblatt PK/PD studies and StatPearls. Individual phase boundaries inferred from PK profile (Tmax ~2h oral, EEG peak ~30 min IV, half-life 10-20h). Confidence medium because no published data specifically decomposes oral subjective phases — the breakdown is inferred from pharmacokinetic parameters. Evidence basis: controlled_human_study
Afterglowtrace	10800–21600 sec(i=0.15)	10800–21600 sec(i=0.15)	medium
Editorial	Phase breakdown derived from work-notes timeline (onset 0-30 min, come_up 30-90 min, peak 1.5-3h, plateau 3-5h, resolution 5-7h, afterglow 7-12+h). Total clinical duration 6-8h from Greenblatt PK/PD studies and StatPearls. Individual phase boundaries inferred from PK profile (Tmax ~2h oral, EEG peak ~30 min IV, half-life 10-20h). Confidence medium because no published data specifically decomposes oral subjective phases — the breakdown is inferred from pharmacokinetic parameters.
	ReasoningReasoning Phase breakdown derived from work-notes timeline (onset 0-30 min, come_up 30-90 min, peak 1.5-3h, plateau 3-5h, resolution 5-7h, afterglow 7-12+h). Total clinical duration 6-8h from Greenblatt PK/PD studies and StatPearls. Individual phase boundaries inferred from PK profile (Tmax ~2h oral, EEG peak ~30 min IV, half-life 10-20h). Confidence medium because no published data specifically decomposes oral subjective phases — the breakdown is inferred from pharmacokinetic parameters. Evidence basis: controlled_human_study

Dose Tier Summaries

thresholdtrace

high

Minimal perceptible anxiolysis emerges as a subtle easing of background tension. Slight muscle relaxation may be noticeable to those with elevated baseline anxiety, while non-anxious users may detect little change. Cognitive function remains largely preserved, with no significant anterograde amnesia expected at this level. Physical effects are minimal — perhaps a faint bodily heaviness or mild sedation that could be mistaken for natural tiredness. Motor coordination is essentially unaffected. The slow blood-brain barrier entry of lorazepam means onset may take 30-45 minutes, making this dose level particularly susceptible to premature redosing if users expect faster effects.

Editorial

Work-notes specify threshold ~0.1 mg with minimal perceptible anxiolysis, slight relaxation, preserved cognition, no significant amnesia. Expanded with BBB delay redosing warning from pharmacokinetic data.

Reasoning

Evidence basis: controlled_human_study

lighttrace

high

Noticeable anxiety suppression and mild sedation define this range. Muscle relaxation becomes apparent, and a general sense of calm settles over mental activity. Thought deceleration begins — racing thoughts slow, and emotional responses feel dampened. Mild anterograde memory impairment is possible but not guaranteed. Physical effects include light bodily heaviness and the beginning of motor control impairment — fine motor tasks may require slightly more concentration. Mild dizziness is possible, particularly when standing quickly. Functional impairment is present but modest. Users may feel capable of normal activities while subtle coordination and reaction-time deficits are already measurable.

Editorial

Work-notes specify noticeable anxiolysis, mild sedation, muscle relaxation, beginning motor coordination effects, mild amnesia possible, emotional blunting begins. Expanded with dizziness from effects profile and functional impairment note.

Reasoning

Evidence basis: controlled_human_study

commontrace

high

Clear anxiety suppression and moderate sedation dominate the experience. Emotional suppression is pronounced — worries, fears, and emotional reactivity feel significantly blunted. Thought deceleration is obvious, with reduced analytical capacity and focus suppression. Anterograde amnesia becomes measurable, lasting up to 6 hours — users may not recall conversations or activities during this window. Muscle relaxation is pronounced. Motor control impairment manifests as noticeable ataxia and slowed reaction time. Physical fatigue and dizziness are common. Appetite enhancement may emerge. Disinhibition and delusions of sobriety are particularly significant at this range — users feel more functional than they objectively are, creating risk for driving, decision-making, and compulsive redosing.

Editorial

Work-notes specify clear anxiolysis, moderate sedation, pronounced muscle relaxation, measurable amnesia up to 6h, motor impairment, thought deceleration, disinhibition, delusions of sobriety. Effects profile confirms amnesia intensity 0.60 and disinhibition 0.50 at common dose.

Reasoning

Evidence basis: controlled_human_study

strongtrace

high

Heavy sedation characterizes this range, with strong hypnotic pressure that may override the user's intention to stay awake. Pronounced anterograde amnesia creates extended blackout windows — activities performed during this period may leave no recoverable memory. Cognitive impairment is severe: decision-making, analysis, and language production are markedly degraded. Motor impairment is significant — walking becomes visibly unsteady, and fine motor tasks are unreliable. Strong muscle relaxation borders on hypotonia. Physical fatigue is heavy, and double vision may occur. Compulsive redosing risk increases substantially at this tier due to the combination of dense amnesia, pronounced disinhibition, and delusions of sobriety — users may take additional doses without remembering previous ones. Non-tolerant users will likely fall asleep.

Editorial

Work-notes specify heavy sedation, pronounced amnesia, significant motor impairment, strong disinhibition, compulsive redosing risk from amnesia+disinhibition, sleep-inducing for non-tolerant users. Expanded with double vision from effects profile.

Reasoning

Evidence basis: controlled_human_study

heavytrace

high

Overwhelming sedation approaching unconsciousness defines this range. Dense anterograde amnesia produces complete blackouts — extended periods with no subsequent recall. Cognitive function is profoundly impaired; coherent speech and purposeful behavior may be impossible. Severe motor impairment makes unassisted movement hazardous. Respiratory depression becomes a clinically significant risk at this dose level, particularly in combination with any other CNS depressant. Aspiration risk increases due to suppressed protective reflexes combined with deep sedation. This dose range carries serious medical risk even without coingestants. The combination of respiratory depression, loss of protective reflexes, and complete amnesia creates conditions where emergency situations may go unrecognized. Medical monitoring is strongly advised.

Editorial

Work-notes specify overwhelming sedation approaching unconsciousness, dense amnesia, severe motor impairment, respiratory depression becomes clinically significant, blackout likely. Safety framing from article prose on high therapeutic index but real respiratory risk at this range.

Reasoning

Evidence basis: controlled_human_study

History

current version

published Oct 2, 2026system—

versions

2 total · since previous: +0 / −0 citations

publication ledger

publish Oct 2, 2026 · by agent-psx

backfill Jun 4, 2026

Historical versions do not record which reviewer approved them; editorial accountability is recorded per value in the database and in the publication ledger going forward.

full version history suggest a correction contact@psychedex.org

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The effects of the nonselective benzodiazepine lorazepam and the α2/α3 subunit-selective GABAA receptor modulators AZD7325 and AZD6280 on plasma prolactin levels
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doi.org/10.1002/cpdd.134 pubmed 27128218no claims checked
[28]
moderate
Management of Alcohol Withdrawal Syndrome in Patients with Alcoholic Liver Disease
Chand PK, Panda U, Mahadevan J, Murthy P · 2022 · Journal of clinical and experimental hepatology
doi.org/10.1016/j.jceh.2022.03.003 pubmed 36340306no claims checked
[29]
weak
Prolonged sedation requiring mechanical ventilation after routine doses of clorazepam - lorazepam preferred in hepatic impairment
Guglielminotti J, Maury E, et al. · 1999 · Intensive care medicine
pubmed 10660854no claims checked
[30]
strong
Comparison of diazepam and lorazepam for the emergency treatment of adult status epilepticus: a systemic review and meta-analysis
Kobata H, Hifumi T, Hoshiyama E, Yamakawa K, Nakamura K, Soh M, Kondo Y, Yokobori S · 2020 · Acute medicine & surgery
doi.org/10.1002/ams2.582 pubmed 33489240no claims checked
[31]
strong
Termination of seizures in the paediatric age group, best benzodiazepine and route of administration: A network meta-analysis
Hasan SU, Pervez A, Bhatty S, Shamim S, et al. · 2022 · The European journal of neuroscience
doi.org/10.1111/ejn.15732 pubmed 35674673no claims checked
[32]
moderate
Sedation in PACU: the role of benzodiazepines
Arcangeli A, Antonelli M, Mignani V, Sandroni C · 2005 · Current drug targets
pubmed 16305452no claims checked
[33]
strong
Clinical Practice Guidelines for the Prevention and Management of Pain, Agitation/Sedation, Delirium, Immobility, and Sleep Disruption in Adult Patients in the ICU (PADIS 2018)
Devlin JW, Skrobik Y, Gélinas C, et al. · 2018 · Critical Care Medicine
doi.org/10.1097/ccm.0000000000003299 pubmed 30113379no claims checked
[34]
moderate
Propylene glycol accumulation in critically ill patients receiving continuous intravenous lorazepam infusions
Horinek EL, Kiser TH, Fish DN, MacLaren R · 2009 · The Annals of pharmacotherapy
doi.org/10.1345/aph.1m313 pubmed 19920159no claims checked
[35]
moderate
The effects of benzodiazepine use during pregnancy and lactation.
McElhatton PR · 1994 · Reproductive toxicology
pubmed 7881198no claims checked
[36]
strong
Effects of tiapride on electroencephalograms and cognitive functions in the elderly
Patat A, Alberini H, Bonhomme D, Soubrane C, Allain H, Gandon JM · 1999 · International clinical psychopharmacology
pubmed 10468312no claims checked
[37]
moderate
Lorazepam and FG 7142 induce tolerance to the DMCM antagonistic effect of benzodiazepine receptor ligands
Petersen EN, Jensen LH · 1987 · Brain research bulletin
pubmed 2824007no claims checked
[38]
moderate
Diazepam-induced loss of inhibitory synapses mediated by PLCδ/Ca2+/calcineurin signalling downstream of GABAA receptors.
Nicholson MW, Sweeney A, Pekle E, et al. · 2018 · Molecular psychiatry
doi.org/10.1038/s41380-018-0100-y pubmed 29904150no claims checked

Claim Verification

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Coverage & Gaps

effect links

55 links · 55 approved · 0 audited0/55 with evidence basis

Lorazepam

Value Provenance

Dosing

oraltrace →

Duration

oral

Safety

Toxicity Profiletrace →

Dependence Profiletrace →

Withdrawal Profiletrace →

Tolerance Profiletrace →

Effects & Profile

Contraindications

Timeline Phases

oral

Dose Tier Summaries

History

Sources

Claim Verification

Coverage & Gaps

oraltrace

Toxicity Profiletrace

Dependence Profiletrace

Withdrawal Profiletrace

Tolerance Profiletrace