International Programme on Chemical Safety
Poisons Information Monograph 464
This monograph is not complete, and the following sections are
included: 1,2,7,9,10,13 and 14.
ATC code: P01BC01 (Anti-protozoals, quinine alkaloids,
Other drugs for disorders of the musculoskeletal
Chinina; Chininum; Quinina;
1.4 Identification numbers
1.4.1 CAS number
1.4.2 Other numbers
Other CAS numbers:
Quinine bisulphate: 549-56-4
Quinine dihydrochloride: 60-93-5
Quinine ethyl carbonate: 83-75-0
Quinine hydrobromide: 549-49-5
Quinine hydrochloride: 130-89-2 (anhydrous)
Quinine hydrochloride: 6119-47-7 (dihydrate)
Quinine sulphate: 804-63-7 (anhydrous)
Quinine sulphate: 6119-70-6 (dihydrate)
ATC Code: M09AA72 (quinine combination with
1.5 Main brand names, main trade names
Adaquin; Bi-Chinine; Biquinate; Biquin (Australia);
Kinin (Sweden); Formula Q (USA)
1.6 Main manufacturers,main importers
To be completed by centre using monograph.
2.1 Main risks and target organs
Cardiotoxicity is usually the cause of death in
Central nervous toxicity includes stupor, delirium, coma, and
Loss of vision and tinnitus or partial/complete deafness.
2.2 Summary of clinical effects
Nausea, vomiting, tinnitus and deafness, headache and
dizziness are early signs of toxicity. Additional toxicity
includes vision disturbances and partial or complete
Vertigo and ataxia may occur.
In severe poisoning: hypotension, delirium, coma,
dysrhythmias, and convulsions are possible.
The most significant toxicity is cardiovascular and includes
sinus tachycardia, high-degree atrioventricular heart block,
prolongation of the PR interval, sinoatrial block and arrest,
ventricular fibrillation, torsade de pointes. Hypotension may
be caused by vasodilation.
Therapeutic doses may give rise to cinchonism, characterized
by tinnitus, headache, nausea, abdominal pain, pruritus, skin
rashes, disturbed vision, and temporary blindness. Acute
renal failure, haemolysis, and thrombocytopenia.
Primarily by history of ingestion and the presence of
typical clinical symptoms: early deafness, tinnitus, vision
disturbances, and cardiac dysrhythmias.
2.4 First aid measures and management principles
Evaluation and support of airway, breathing, and
circulation. Activated charcoal and intensive monitoring of
cardiovascular function is necessary. Induction of emesis is
Chemotherapy of malaria, especially in
chloroquine-resistant malaria and cerebral malaria
(White & Warrel, 1983; Hall & Peters, 1985).
For nocturnal leg cramps.
In patients with myotonia.
Heroin may be diluted with quinine (Lupovich et al.,
Quinine has often been used as an abortifacient. It
has also been used has antipyretic and analgesic.
Tonic water contains approximately 80 mg/L quinine
sulphate as a flavouring agent.
4.2 Therapeutic dosage
Oral treatment: 600 to 650 mg three times daily for at
least 3 days (USP; Reynolds, 1996), usually as the
sulphate, hydrochloride, or dihydrochloride. These 3
salts contain approximately the same amount of quinine
and any of them can be used when the dose is cited in
terms of "quinine salts" (Reynolds, 1996).
The usual dosage of totaquine for malaria is 600 mg
three times daily after meals (Webster, 1990).
Intravenous: initial loading dose of 7 mg/kg of
quinine dihydrochloride given over 30 minutes followed
immediately by maintenance infusions, or an initial
dose of 20 mg/kg (up to a maximum of 1.4 g) given over
4 hours with maintenance infusions being started 8 to
12 hours later. Maintenance infusions: 10 mg/kg (up to
a maximum of 700 mg) given over 4 hours every 8 to 12
hours. If parenteral therapy is required for more than
48 hours the dose should be reduced by one-third or
one-half. Monitor carefully for signs of
cardiotoxicity. Therapy should be changed to oral
administration as soon as possible to complete the
If intravenous infusion is not possible, quinine
dihydrochloride may be given intramuscularly where
doses, including the loading dose are the same as
those used for intravenous administration (Reynolds,
Nocturnal leg cramps:
Recumbency leg muscle cramps (night cramps) are
reportedly relieved by quinine. The usual quinine
sulphate dose is 200 to 300 mg, which may be repeated
once before retiring. In some individuals, only a
brief period of quinine therapy is required to provide
relief; while even large doses of the drug are
ineffective in others (Webster, 1990).
Oral treatment: 10 mg of quinine salt per kg
body-weight 3 times a day (Reynolds, 1996).
Quinine is contraindicated in patients with a history of
hypersensitivity and in the presence of haemoglobinuria
during malaria and in patients with optic neuritis, or
tinnitus (Reynolds, 1996).
It should be used with caution in patients with atrial
fibrillation and other myocardial conduction
Quinine may enhance the effects of anticoagulants.
In patients with myasthenia, quinine may cause severe
respiratory distress and dysphagia.
In patients with glucose-6-phosphate deficiency, blackwater
fever may be observed when quinine is used (Reynolds,
7. PHARMACOLOGY AND TOXICOLOGY
7.2.1 Human data
Toxicity is observed after overdoses
of 2.5 to 4 g (Murray & Jay, 1983).
Adverse effects are not dose-related.
Toxicity is described above 25 mg/kg
in children. Fatalities have occured at the
900 mg dose in children aged 1 to 2 years
(Winek et al., 1974; Grattan-Smith et al.,
9. CLINICAL EFFECTS
9.1 Acute poisoning
In a series of overdoses with quinine in
adults, 75% of patients were symptomatic, 17% had
visual symptoms, and 50% had adverse cardiovascular
effects (Dyson et al., 1985)
In a review of 16 quinine overdose patients, 9
patients had reversible or irreversible visual damage,
3 had cardiac arrhythmias and one death was reported
(Bateman et al., 1985).
The patient may present with stupor, coma, confusion,
delirium or have extensive muscle weakness.
Convulsions can occur (Wolf et al., 1992).
9.1.3 Skin exposure
9.1.4 Eye contact
9.1.5 Parenteral exposure
When administered intravenously it may produce
venous thrombosis. Intramuscular and subcutaneous
injection can result in tissue necrosis.
The clinical toxicity is the same as in oral
administration, and the onset is more rapid.
9.2 Chronic poisoning
Toxicity includes central nervous system (CNS),
cardiovascular, gastrointestinal (GI), dermatologic,
hematologic and renal toxicity. Cinchonism may occur
with therapeutic doses (Reynolds, 1996). Progressive
visual loss following ingestion of excessive amounts
of Indian tonic water has been reported (Horgan &
9.2.3 Skin exposure
No data available.
9.2.4 Eye contact
No data available.
9.2.5 Parenteral exposure
No data avilable.
9.3 Course, prognosis, cause of death
The major causes of morbidity in quinine overdose
include reversible renal failure, cinchonism, prolonged
hearing deficits, and blindness; the skin is often hot and
flushed initially then may become cold and pale (Rollo, 1975;
Dannenberg et al., 1983; Licciardello & Stanbury, 1984;
Medical letter, 1984; Marr, 1985; Reynolds, 1993;
McEvoy,1994). Death generally follows cardiac disturbances,
renal failure, acute haemolytic anaemia and respiratory
arrest (Dannenberg et al., 1983; Licciardello & Stanbury,
9.4 Systematic description of clinical effects
Quinine has a negative inotropic action, it
slows the rate of depolarization and conduction, and
increases the action potential duration and the
effective refractory period in the myocardium (Bateman
& Dyson, 1986; Mack, 1986; Jaeger et al., 1987).
Prolongation of the PR, QT, and QRS intervals, ST and
T waves changes, and U waves may be observed (Bateman
& Dyson, 1986; Smilkstein et al., 1987; Goldfrank &
Osborn, 1990,). SA block/arrest, high degree AV block,
complete AV dissociation, ventricular tachycardia,
ventricular fibrillation, and torsade de pointes are
reported (Boland et al., 1985; Bateman & Dyson et al.,
1986; Smilkstein et al., 1987; Goldfrank & Osborn,
Quinine has an alpha-adrenergic blocking effect and
hypotension may occur as result of vasodilation,
myocardial depression, or dysrhythmias (Bateman &
Dyson, 1986; Goldenberg & Wexler, 1988). Bradycardia
rarely occurs due to vagolytic activity (Smilksten et
Bodenhamer & Smilkstein (1993) reported a quinine
overdose resulting in the delayed onset of cardiac
ventricular conduction defects, ectopy, and torsade de
pointes and subsequent cardiac arrest 25 hours after
Quinine administered intravenously may produce venous
Initially increased, later shallow and
220.127.116.11 Central Nervous System (CNS)
In severe poisonings, headache,
fever, vomiting, excitement, confusion,
delirium, syncope, lowering of the body
Vertigo and ataxia, with presumed involvement
of the vestibular nerve may occur (Bateman &
18.104.22.168 Peripheral nervous system
No data available.
22.214.171.124 Autonomic nervous system
No data available.
126.96.36.199 Skeletal and smooth muscle
Quinine increases the tension
response to a single maximal stimulus
delivered to the muscle directly or through
the nerve, but it also increases the
refractory period of the muscle so that the
response to tetanic stimulation is
diminished. The excitability of the motor
end-plate region decreases so that responses
to repetitive nerve stimulation and to
acetylcholine are reduced. Thus, quinine can
antagonize the actions of physostigmine on
skeletal muscle as does curare. The same
mechanism, however, may provoke alarming
respiratory distress in patients with
myasthenia gravis (Webster, 1990).
On uterine muscle it may be oxytocic to the
pregnant uterus (Rollo, 1975).
Nausea, vomiting, abdominal pain, and diarrhea
result from the local irritant action of quinine.
Nausea and vomiting may also be secondary to a CNS
mechanism. (Goodman & Gilman, 1990).
Granulomatous hepatitis has been reported (Katz
et al., 1983; Mathur et al., 1990); cholestatic and
hepatocellular toxicity, probably secondary to a
hypersensitivity reaction, has also been
Tubular obstruction, acute renal
failure (Winek et al., 1974; Bateman & Dyson,
No data vailable.
9.4.7 Endocrine and reproductive system
Therapeutic doses of quinine may lower blood
glucose concentrations by stimulating insulin
secretion (Looareesuwan et al., 1985; Okitolonda et
Recurrent hyperinsulinemic hypoglycaemia can be
particularly serious when quinine is used during
pregnancy or when there is severe infection (Webster,
Symptomatic hypoglycaemia has been reported (Browne &
Coppel, 1984; Limburg et al., 1993).
It has been reported to decrease male reproductive
Use of quinine as an abortifacient can produce
poisoning in the fetus with frequent infant deafness
(Dannenberg et al., 1983).
The skin may be hot, flushed and sweating.
Rashes frequently appear.
Angioedema, especially of the face, may be observed.
The skin becomes cold and cyanotic as the poisoning
progresses (Webster, 1990).
9.4.9 Eye, ear, nose, throat: local effects
Ear: Transient hearing loss, usually a first
side effect, occurs a few hours after initiating high-
dose therapy (up to 2 g in the treatment of malaria).
After prolonged daily courses of 200 to 300 mg, up to
20% of patients can be expected to suffer from hearing
loss (Miller, 1985). The sensorineural hearing loss is
typically reversible, bilateral, and symetric,
affecting the high frequencies first (4, 6, and 8 kHz)
with a characteristic 4-kHz notch (Roche et al.,
Discrimination scores have been noted to fall below
30% (Koegel, 1985).
Ototoxicity of quinine is probably secondary to direct
cochlear hair cell damage (Rybak, 1985). Vertigo and
ataxia secondary to presumed involvement of the
vestibular nerve may occur (Bateman & Dyson,
Eye: as early as 15 to 30 mn after a quinine
overdose the patient may complain of a blurred
The mean time of onset of blindness is 6 hours, while
usually gradual, can be sudden.
It may pass after 14 to 24 hours, however it may last
up to 10 weeks or longer.
Generally there is full recovery in 1 to 3 weeks,
however patient may become permanently blind.
Ophtalmic findings during the acute phase are dilated
pupils and unresponsiveness to light in proportion to
the degree of blindness. The ophthalmoscopic
appearances have varied considerably from case to case
and this has occasioned much dispute concerning the
mechanism by which vision is affected. In some cases
the retinal vessels have appeared narrowed early. In
another group of cases the retina has appeared
oedematous and the papilla hyperaemic. Occasionally a
red spot in the macula has been noted with oedema. In
yet other cases the fundi have appeared normal at an
early stage while the patient was already profoundly
blind. It has been reported very frequently that at a
later stage, after some days or weeks, the retinal
arterioles have become strikingly narrowed, often at a
time when central vision had returned, or was
returning. Pallor of the optic nerve heads has often
been noted, developing gradually, generally
proportional to the amount of permanent loss of visual
field (Grant, 1986).
In the acute stages of loss of vision, the
electroretinogram may be normal. Thereafter it becomes
abnormal during the phase of visual improvement and
parallels the changes of visual acuity on the second
or third day.
Visual evoked potentials, dark adaptation, and color
testing measurements are often abnormal (Ellenhorn et
Visual loss was observed in a patient who was drinking
4 liters of tonic water each day for 12 months prior
to presentation. Retinal vessels were of normal
calibre but each macula exhibited fine stippling shown
by fluorescein angiography (Horgan & Williams,
Quinine-induced agranulocytosis has been
reported. It has been confirmed by the inhibition,
in vitro, of bone-marrow cell cultures by
therapeutic concentrations of quinine (Sutherland et
Other abnormalities include: Coombs' positive
haemolytic anaemia, neutropenia, dissiminated
intravascular coagulation, hypoprothrombinaemia, and
thrombocytopenia (Belkin, 1976; Pfueller et al., 1988;
Spearing et al., 1990; Hagley et al., 1992; Aster,
1993; Maguire et al., 1993).
Haemolysis can result when quinine is administered to
patients with G6PD deficiency.
No data available.
188.8.131.52 Acid-base disturbances
Secondary to respiratory
insufficiency and renal disturbances,
seizures and cardiovascular
184.108.40.206 Fluid and electrolyte disturbances
Secondary to renal dysfunction.
No data available.
9.4.13 Allergic reactions
Some patients are hypersensitive to quinine
and even small doses may give rise to symptoms of
cinchonism, together with angioneurotic oedema, asthma
and other allergic phenomena (Barr et al., 1990).
Haemolytic anaemia and thrombocytopenia have been
reported. As a test for quinine idiosyncrasy a scratch
test may be made with a 1 to 10% solution of a quinine
salt in physiological saline: redness, oedema, and
itching occur within 5 to 15 minutes if the patient is
hypersensitive (Reynolds, 1982).
Photosensitivity reactions following systemic
administration (Reynolds, 1996).
9.4.14 Other clinical effects
No data available.
No data available.
10.1 General principles
Admission in an intensive care department is indicated.
Monitoring the airway, breathing, and circulation.
Gastrointestinal decontamination with activated charcoal
should be undertaken.
10.2 Life supportive procedures and symptomatic/specific treatment
After basic support of airway, breathing, and
circulation, vasopressors and specific treatment of
conduction disorders may be required. Antiarrhythmics that
depress conduction (Class IA) should be avoided, ie
quinidine, procainamide. Sodium bicarbonate may be used,
fluids and electrolyte administration may be required.
Early gastric decontamination should be used. The use
of ipecac should be avoided, and gastric lavage used only for
recent/large ingestion. Activated charcoal is very effective
and should be the primary method of gastric
10.4 Enhanced elimination
Efficacy of elimination procedures is limited by the
extensive protein binding and volume of distribution (Maher,
1983). Acidification of urine is not recommended, as it does
increase cardiotoxicity. Forced diuresis is not effective.
Early resin haemoperfusion may be effective in severe
poisoning. In later phases of poisoning, haemoperfusion,
haemodialysis or peritoneal dialysis are not effective.
Exchange transfusion has not been successful (Bateman et al.,
10.5 Antidote treatment
10.6 Management discussion
The treatment of cardiac dysrhythmias with bicarbonate
or lactate counteracts the elimination of quinine. The
elimination of quinine in acidic urine is two times higher
than in alkaline urine, but not clinically important.
The treatment of quinine amblyopia is controversial. Because
the etiology was originally thought to be retinal ischaemia,
multiple methods have been used to cause retinal
vasodilation. Stellate ganglion block, retrobulbar injection
of vasodilators, and anterior chamber paracentesis have all
generally been found to be ineffective in the treatment of
quinine-induced blindness (Gangitano & Keltner, 1980; Dyson
et al., 1985; Smilkstein et al., 1987; Canning & Hague,
1988). Stellate ganglion block has been associated with
serious complications, including death (Adriani et al.,
Hyperbaric oxygen, hemodialysis, and resin hemoperfusion have
been suggested to be effective in the treatment of blindness
refractory to other therapy.
Adriani J, Parmley J, Ochsner A (1952) Fatalities and
complications after attempts at stellate ganglion block. Surgery
Aster RH (1993) Quinine sensitivity: a new cause of the hemolytic
uremic syndrome. Ann Intern Med 119: 243-244
Barr E, Douglas JF, Hill CM (1990) Recurrent acute
hypersensibility in quinine. B M J 301: 323.
Bateman D & Dyson EH (1986) Quinine toxicity. Adv Drug React Ac
Pois Rev 5: 215-233.
Bateman DN, Blain PG, Woodhouse KW (1985) Pharmacokinetics and
clinical toxicity of quinine overdosage: Lack of efficacy of
techniques intended to enhance elimination. Q J Med N Ser
Belkin GA (1976) Cocktail purpura. An unusual case of quinine
sensitivity. Ann Intern Med 66: 583.
Bodenhamer JE & Smilkstein MJ (1993) Delayed cardiotoxicity
following quinine overdose:a case report. J Emerg. Med 11:
Boland ME, Roper SMG, Henry JA (1985) Complications of quinine
poisoning. Lancet I: 384-385.
Browne GF & Coppel DL (1984) Management of quinine overdose. Hum
Toxicol 3: 399-402.
Canning CR & Hague S (1988) Ocular quinine toxicity. Br J
Ophthalmol 72: 23-26.
Dannenberg AL, Dorfman SF, Johnson J (1983) Use of quinine for
self induced abortion. South Med J 76: 846-849.
Dyson EH, Proudfoot AT, Bateman DN (1985-1986) Quinine amblyopia:
is current management appropriate? Clin toxicol 23: 571-578.
Dyson EH, Proudfoot AT, Prescott LF, Heyworth R (1985) Death and
blindness due to overdose of quinine. Br Med J 291: 31-33.
Ellenhorn MJ & Barceloux DG (1988) Medical Toxicology- Diagnosis
and Treatment of Human Poisoning. Elsevier, New York, NY.
Ellenhorn MJ, Schonwald S, Ordog G, Wasserberger (1997) "Quinine"
in Ellenhorn's Medical Toxicology 2nd,ed. Williams & Wilkins,
Baltimore. pp 294-295.
Gangitano JL & Keltner JL (1980) Abnormalities of the pupil and
visual-evoked potential in quinine amblyopia. Am J Ophthalmol 89:
Goldenberg AM & Wexler LF (1988) Quinine overdose: review of
toxicity and treatment. Clin Cardiol 11: 716-718.
Goldfrank LR & Osborn H (1990) Quinine. In LR Goldfrank, NE
Flowenbaum, NA Lewin, RS Weisman, MA MA Howland, eds. East
Norwalk, CT. Appleton and Lange pp 337-340.
Grant WM (1986) Toxicology of the Eye. 3rd ed. C.C Thomas (ed).
Grattan-Smith TM, Gillis J, Kilham A (1987) Quinine poisoning in
children Med J Aust 147: 92-95.
Hagley MT, Hosney IA, Hulisz DT, Hayes HD (1992) Hemolytic-uremic
syndrme associated with ingestion of quinine. Am J Nephrology 12:
Hall A (1985) Dangers of high dose quinine and overhydration in
severe malaria. Lancet I: 1453.
Hall AP & Peters W (1985) The treatment of severe falciparum
malaria. Brit Med J 291: 1146-1147.
Horgan SE & Williams RW (1995) Chronic retinal toxicity due to
quinine in Indian Tonic water Eye 9: 637-638.
Jaeger A, Sauder P, Kopferschmitt J, Flesch F (1987) Clinical
faetures and management of poisoning due to antimalarial drugs.
Med Tox 2: 242-273.
Katz B, Weetch M, Chopra S (1983) Quinine-induced granulomatous
hepatitis. BMJ 286: 264-265.
Koegel L Jr (1985) Ototoxicity: A contemporary review of
aminoglycosides, loop diuretics, acetylsalicylic acid, quinine,
erythromycin, and cisplatinum.Am J Otol 6: 190-199.
Licciardello AT & Stanbury JB (1984) Acute hemolytic anaemia from
quinine used as an abortifacient. N Engl J Med 238: 120-121.
Limburg PJ, Katz H, Grant CS, Service FJ (1993) Quinine induced
hypoglycemia. Ann Intern Med 119: 218-219.
Lupovich P, Pilewski R,Sapira JD (1970) Cardiotoxicity of quinine
as adulterant in drugs. JAMA 212: 216.
Looareesuwan S, Philips RE, White NJ, Kietinun S, Karbwang, Rackow
C, Turner RC,Warrell DA (1985) Quinine and severe falciparum
malaria in late pregnancy. Lancet 2: 4-8.
Mack RB (1986) Quinine poisoning: rage against the dying of the
light. N C Med J 47: 263-264.
Maguire RB, Stroncek DF, Campbell AC (1993) Recurrent
pancytopenia, coagulopathy, and renal failure associated with
multiple quinine-dependent antibodies. Ann Internal Med
Maher JF (1983) Pharmacological aspects of renal failure and
dialysis, in W.Drukker, FM Parsons, JF Maher (Eds): Replacement of
Renal Function by Dialysis. Martinus Nijhoff, Boston. p. 770.
Marr JJ (1985) Antiparasitic agents. In: GL Mandell, RG Douglas,
JE Bennet, eds. Anti-infective Therapy. Wiley, New York:
Mathur S, Dooley J, Scheuer PJ (1990) Quinine induced
granulamatous hepatitis and vasculitis BMJ 300: 613
McEvoy GK, ed. (1994) Quinine, in AHFS Drug In formation 94,
American Society of Hospital Pharmacists, Bethesda, MD
Medical Letter (1984) Handbook of Antimicrobal Therapy. rev ed.
New Rochelle New York p. 101.
Miller JJ (ed) (1985): Antimalarial drugs. In CRC Press, pp 9-15.
Murray SF & Jay JL (1983) Loss of sight after self poisoning with
Quinine. Br Med J 287: 1700.
Okitolonda W, Delacollette C, Mallengrean M, Henquin JC (1987)
Hogh incidence of hypo-glycaemia in African patients treated with
intravenous quinine for severe malaria. Br Med J 295: 716-718.
Pfueller SL, Bilston RA, Logan D, Gibson JM, Firkin BG (1988)
Heterogeneity of drug-dependent platelet antigens and their
antibodies in quinine- and quinidine-induced thrombocytopenia:
involvement of glycoproteins Ib, Iib, IIIa, and IX. Blood 72:
Reynolds (1982) The Extra Pharmacopoeia 28 Edition. J.E.F.
Reynolds. A.B. Prasad (Eds.) The Pharmaceutical Press. London.
Reynolds (1996) The Extra Pharmacopoeia, 31 Ed. JEF Reynolds. The
Pharmaceutical Press, London
Roche RJ, Salimut K, Pikrittayakamee S, Molunto P, Boonamrung S,
White NJ (1990) Quinine induces reversible high tone hearing loss.
Br J Clin Pharmacol 29: 780-782.
Rollo IM (1975) Drugs used in the chemotherapy of malaria. In:
Goodman LS, Gilman A,eds The Pharmacological Basis of
Therapeutics. 5th ed. MacMillan NewYork p.p. 1062-1065.
Rybak L (1986) Drug ototoxicity. Ann Rev Pharmacol Toxicol
Smilkstein MJ, Kullig KW, Rumack BH (1987) Acute toxic blindness;
unrecognized quinine poisoning. Ann Emerg Med 16: 98-101.
Spearing RL, Hickton CM, Sizeland P, Hannah A, Bailey (1990)
Quinine-induced desseminated intravascular coagulation. Lancet
Sutherland R, Vincent PC, Raik E, Burgess K (1977) Quinine induced
agranulucytosis: toxic effect of quinine bisulphate on bone marrow
in vitro. Br Med J 1: 605-607.
Webster LR Jr (1990) Drugs used in chemotherapy of protozoal
infections. Malaria. In Goodman and Gilman's The Pharmacological
Basis of Therapeutics. 8th Edition. A.Goodman Gilman, TW Rall,
A.S.Nies, P.Taylor (Eds) Pergamon Press, New York.
White NJ & Warrell DA (1983) Clinical management of chloroquine
resistant plasmodium falciparum malaria in Southeast Asia. Trop
Doct 13: 153-158.
Windholz M (1976) The Merck Index, 9th edition. Merck & Co, Inc,
Winek CL, Davis ER, Collom WD, Shanon SP (1974) Quinine fatality-
Case report. Clin Toxicol 7: 129-132.
Wolf LR, Otten EJ, Spadafora MP (1992) Cinchonism: Two case
reports and review of acute quinine toxicity and treatment.
J Emerg Med 10: 295-301.
14. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES)
Author: Prof. Dr. A.N.P. van Heijst
Baarnseweg 42 A
3735 MJ Bosch en Duin
Tel: (31) (30) 228 71 78
Fax (31) (30) 225 13 68
Date: January 1997
Reviewer: MO Rambourg Schepens
Centre Anti-Poisons de Champagne Ardenne
Centre Hospitalier Universitaire
F-51092 Reims Cedex
Date: August 1997
Peer review: INTOX-10 Meeting, Rio, Brazil September, 3rd, 1997
(Drs M Kowalczyk, L Lubomirov, R Mc Keown, P Rosen, W Watson)
Finalization: MO Rambourg Schepens/M Ruse