LBM 6

Toxidrom : sebuah sindrome yang disebabkan oleh adanya racun dalam tubuh

STEP 2

1. Apa saja zat atau toxin yang tergandung dalam bunga trompet (brugmansia suaveolens)?
2. Apa saja tanda dan gejala toxidrom?
3. Mengapa didapatkan pemeriksaan tanda vital seperti di skenario?
4. Mengapa pasien tampak gelisah, bingung, muntah-muntah?
5. Mengapa pada pemeriksaan fisik di dapatkan mata diameter pupil 6mm, reflek cahaya
(++), mulut tampak kering, ekstremitas kulit tampak kemerahan dan hangat
6. Bagaimana patofisiologi efek toksik anti kolinergik di sistem saraf pusat dan otonom?
7. Bagaimana penatalaksanaan yg tepat pada kasus keracunan terutama pada keracunan
bunga terompet?
8. Apa saja pemeriksaan penunjang dari skenario?
9. Apa saja gejala dan tanda dari pasien boleh dipulangkan dari IGD?
10. Bagaimana mekanisme masuknya racun ke tubuh?
11. Apa saja komplikasi dari intoksikasi?
12. Macam-macam toksin yg menyebabkan ssp dan autonom

STEP 3

1. Mengapa pasien tampak gelisah, bingung, muntah-muntah?

Central mus- carinic blockade effects depend on the offending
agent’s ability to per- meate the blood-brain barrier. For example,
atropine and scopolamine possess a tertiary amine group that
allows these compounds to cross the blood-brain barrier and cause
central nervous system activity
Sumber : Diagnosis and treatment of drug-induced hyperthermia
Megan e. MusselMan and suprat saely
 SUMBER : Muscarinic Blocking Drugs, William F Wonderlin

2. Mengapa pada pemeriksaan fisik di dapatkan mata diameter pupil 6mm, reflek cahaya
(++), mulut tampak kering, ekstremitas kulit tampak kemerahan dan hangat, abdomen
MIDRIASIS, MULUT KERING, KULIT KEMERAHAN, BISING USUS MENURUN
SUMBER : Muscarinic Blocking Drugs, William F Wonderlin

HYPOHIDROSIS
SUMBER : Drug-Induced Hyperhidrosis and Hypohidrosis: Incidence, Prevention and
Management, William P. Cheshire Jr and Robert D. Fealey
HIPERTERMI
 Pathophysiology. Hyperthermia is caused by the blockade of both central and peripheral
muscarinic, acetylcholine receptors. Therefore, anticholinergic poisoning is often- times
referred to as antimuscarinic poisoning syndrome. Central mus- carinic blockade effects
depend on the offending agent’s ability to per- meate the blood-brain barrier. For
example, atropine and scopolamine possess a tertiary amine group that allows these
compounds to cross the blood-brain barrier and cause central nervous system activity.
Conversely, other agents, such as glycopyrro- late, contain a quaternary amine group that
impairs the ability of the compound to cross the blood-brain barrier, and only peripheral
adverse effects are seen. Peripheral mus- carinic blockade by anticholinergic agents
interferes with cutaneous heat loss by impairing sweat-gland func- tion. In such cases,
hyperthermia results from the combination of heat production from increased muscle
activity and the inability to dissipate heat through sweating.
SUMBER : Diagnosis and treatment of drug-induced hyperthermia, Megan e. MusselMan
and suprat saely

3. Mengapa didapatkan pemeriksaan tanda vital seperti di skenario?

 The heart rate increases (tachycardia) with hypertension as a result of
parasympathetic block caused by anti-cholinergic agents.
SUMBER : Effects of Atropa belladonna as an Anti-Cholinergic, Hemangi Rajput*

SUMBER : Muscarinic Blocking Drugs, William F Wonderlin

4. Bagaimana mekanisme masuknya racun ke tubuh?

 SUMBER : EIMED PAPDI

5. Apa saja tanda dan gejala toxidrom?

 SUMBER : Goldfrank’s Manual of Toxicologic Emergencies

6. Apa saja zat atau toxin yang tergandung dalam bunga trompet (brugmansia suaveolens)?
The plant Atropa belladonna is a perennial herb belonging to the family
Solanaceae. The intoxication is caused by the alkaloids atropine, scopolamine and
hyoscyamine, which are present in the berries, leaves and roots. The intoxication
causes anti-cholinergic effects on the body causing anti-cholinergic toxidrome
SUMBER : Effects of Atropa belladonna as an Anti-Cholinergic, Hemangi Rajput

7. Bagaimana patofisiologi efek toksik anti kolinergik di sistem saraf pusat dan otonom?

Effect of Atropa belladonna on the central nervous system

The Atropa belladonna alkaloids atropine and scopolamine are known to be

antagonist for muscarinic receptors. They block the muscarinic receptor
acetylcholine, which plays an important role in the functioning of the brain for
 learning, memory and orientation. In the event of the muscarinic blockade, the
absence of acetylcholine causes dysfunctional memory, disorientation and
hallucination [2]. The respiratory rate increases and in some cases of overdose,
leads to respiratory and cardiovascular failure [7,8].

Effect of Atropa belladonna on peripheral nervous system

The alkaloid atropine acts as muscarinic antagonist and blocks the parasympathetic
postganglionic muscarinic receptors [1,2,6]. Atropine has a stronger effect than
scopolamine in producing tachycardia and cardiovascular changes, although the
peripheral effects of both atropine and scopolamine are the same [9,10]. The signs
of peripheral effects manifested by the parasympathetic block include decreased
secretions causing dryness of mouth, ushed skin, mydriasis, vomiting, constipation,
urinary retention, fever, tachycardia and hypertension [1,2].

SUMBER : Effects of Atropa belladonna as an Anti-Cholinergic, Hemangi Rajput

8. Bagaimana penatalaksanaan yg tepat pada kasus keracunan terutama pada keracunan

bunga terompet?

Jelaskan farmakodinamik antidotum

Physostigmine is a carbamate that inhibits the enzyme cholinesterase within the body,
resulting in elevated acetylcholine concentrations at nerve end plates. This rise in
acetylcholine concentrations can overcome cholinergic receptor blockade at both central
and peripheral nerve terminals, and reverse many anticholinergic effects. Physostigmine
can be considered for two main instances in the treatment of severe anticholinergic
intoxication. First, physostigmine can be used to support the clinical diagnosis of
anticholinergic poisoning. A patient may present without a clear history of anticholinergic
plant or medication exposure, but may display the classic physical examination findings
listed above. A “diagnostic challenge” with a bolus dose of physostigmine may reverse
those signs and symptoms of toxicity, especially in the central nervous system, thus
confirming the diagnosis and avoiding a more extensive and time-consuming work up for
altered mental status. Secondly, physostigmine can be considered for cases of
anticholinergic poisoning with features refractory to conventional management, such as
intractable seizures or prolonged agitation. All patients receiving physostigmine should be
placed on a cardiac monitor with pulse oximetry, and the drug should be administered in
slow, graduated doses by a bedside physician. Physostigmine is dosed in 0.5-1.0 mg
increments every 5-10 minutes up to a maximum of 2.0 mg. Atropine should be available
at bedside for any patient receiving physostigmine since bradycardia can occur. Patients
exposed to tricyclic antidepressants and patients with cardiac conduction delays, such as
a widened QRS interval, should not receive physostigmine

SUMBER : Anticholinergic Plants, Volume 6, Number 4 Winter 2008

Indications for the use of physostigmine include the presence of peripheral or central
anticholinergic manifestations without evidence of QRS or QTc pro- longation. Peripheral
anticholinergic manifestations include dry mucosa, dry skin, flushed face, mydriasis,
hyperthermia, decreased bowel sounds, urinary retention, and tachycardia. Central
anticholinergic manifestations include ag- itation, delirium, hallucinations, seizures, and
coma. The relative contraindi- cations to physostigmine use include reactive airways
disease, peripheral vas- cular disease, intestinal or bladder obstruction, intraventricular
conduction defects, and atrioventricular (AV) block.

SUMBER : Goldfrank’s Manual of Toxicologic Emergencies

Kerja asetilkolin di ssp secara fisiologis

ACETYLCHOLINE

Acetylcholine (ACh) is a neurotransmitter of the central and peripheral ner- vous

system. Centrally, it is found in both brain and spinal cord; cholinergic fibers
project diffusely to the cerebral cortex. Peripherally, ACh serves as a
neurotransmitter in autonomic and somatic motor fibers (Fig. 14–1).

Synthesis, Release, and Inactivation

Acetylcholine is synthesized from acetylcoenzyme A and choline. Acetyl- choline

undergoes degradation in the synapse to choline and acetic acid by
acetylcholinesterase. Pseudocholinesterase (plasma cholinesterase) plays no role in
the degradation of synaptic ACh metabolism. However, it does metab- olize some
drugs, including cocaine and succinylcholine.

Acetylcholine Receptors

After release from cholinergic nerve endings, ACh activates two main types of
receptors: nicotinic and muscarinic (Fig. 14–1).

Nicotinic Receptors

Nicotinic receptors (nAChRs) reside in the CNS (mainly in spinal cord), on post-
ganglionic autonomic neurons (both sympathetic and parasympathetic), and at
skeletal neuromuscular junctions, where they mediate muscle contraction.

Muscarinic Receptors

Muscarinic receptors reside in the CNS (mainly in the brain), on end organs
innervated by postganglionic parasympathetic nerve endings, and at most
postganglionic sympathetically innervated sweat glands (Fig. 14–2).
SUMBER : Goldfrank’s Manual of Toxicologic Emergencies

Penanganan awal keracunan

 SUMBER : Goldfrank’s Manual of Toxicologic Emergencies

9. Apa saja pemeriksaan penunjang dari skenario?

10. Apa saja gejala dan tanda dari pasien boleh dipulangkan dari IGD?
11. Apa saja komplikasi dari intoksikasi?

STEP 4