Adjunctive treatment of alcohol and opioid withdrawal
Agitation and confusion associated with cerebral sclerosis
Alcohol-induced psychosis
Hallucinations in alcohol withdrawal
Hyperactive delirium (to control the agitation component of delirium)
Hyperactivity, aggression
Otherwise uncontrollable, severe behavioral disorders in children and adolescents
Schizophrenia
Therapeutic trial in personality disorders, such as borderline personality disorder
Treatment of intractable hiccups
Treatment of neurological disorders, such as tic disorders such as Tourette syndrome, and chorea
Treatment of severe nausea and emesis in postoperative and palliative care, especially for palliating adverse effects of radiation therapy and chemotherapy in oncology. Also used as a first line antiemetic for acute Cannabis Hyperemesis Syndrome.Haloperidol was considered indispensable for treating psychiatric emergency situations, although the newer atypical drugs have gained a greater role in a number of situations as outlined in a series of consensus reviews published between 2001 and 2005.In a 2013 comparison of 15 antipsychotics in schizophrenia, haloperidol demonstrated standard effectiveness. It was 13–16% more effective than ziprasidone, chlorpromazine, and asenapine, approximately as effective as quetiapine and aripiprazole, and 10% less effective than paliperidone. A 2013 systematic review compared haloperidol to placebo in schizophrenia:

Pregnancy and lactation
Data from animal experiments indicate haloperidol is not teratogenic, but is embryotoxic in high doses. In humans, no controlled studies exist. Reports in pregnant women revealed possible damage to the fetus, although most of the women were exposed to multiple drugs during pregnancy. In addition,  reports indicate neonates exposed to antipsychotic drugs are at risk for extrapyramidal and/or withdrawal symptoms following delivery, such as agitation, hypertonia, hypotonia, tremor, somnolence, respiratory distress, and feeding disorder.
Given that antagonism of D2 receptors is more beneficial on the positive symptoms of schizophrenia and antagonism of 5-HT2 receptors on the negative symptoms, this characteristic underlies haloperidols greater effect on delusions, hallucinations and other manifestations of psychosis. Haloperidols negligible affinity for histamine H1 receptors and muscarinic M1 acetylcholine receptors yields an antipsychotic with a lower incidence of sedation, weight gain, and orthostatic hypotension though having higher rates of treatment emergent extrapyramidal symptoms. Haloperidol acts on these receptors: (Ki)

D1 (silent antagonist) – Unknown efficiency
D5 (silent antagonist) – Unknown efficiency
D2 (inverse agonist) – 0.7 nM
D3 (inverse agonist) – 0.2 nM
D4 (inverse agonist) – 5–9 nM
σ1 (irreversible inactivation by haloperidol metabolite HPP+) –  3 nM
σ2 (agonist): 54 nM
5HT1A receptor agonist –  1927 nM
5HT2A (silent antagonist) –  53 nM
5HT2C (silent antagonist) – 10,000 nM
5HT6 (silent antagonist) – 3666 nM
5HT7 (irreversible silent antagonist) – 377.2 nM
H1 (silent antagonist) – 1,800 nM
M1 (silent antagonist) – 10,000 nM
α1A (silent antagonist) – 12 nM
α2A (silent antagonist) – 1130 nM
α2B (silent antagonist) – 480 nM
α2C (silent antagonist) – 550 nM
NR1/NR2B subunit containing NMDA receptor (antagonist; ifenprodil site): IC50 – 2,000 nM

Pharmacokinetics
By mouth
The bioavailability of oral haloperidol ranges from 60 to 70%. However, there is a wide variance in reported mean Tmax and T1/2 in different studies, ranging from 1.7 to 6.1 hours and 14.5 to 36.7 hours respectively. Intramuscular injections
The drug is well and rapidly absorbed with a high bioavailability when injected intramuscularly. The Tmax is 20 minutes in healthy individuals and 33.8 minutes in patients with schizophrenia.