INTOKSIKASI

Penyebab intoksisasi ada banyak macam, yang sering terjadi adalah karena
kecelakaan atau, disengaja / bunuh diri. Di Amerika intoksikasi ± 75% terjadi pada
anak umumnya karena keracunan produk rumah tangga

A. Agen Intoksikasi
Terjadi pada semua umur remaja: obat-obat psikotropik, sedative, transqualizer,
antidepresan dan obat-obat narkotik. dewasa umumnya karena kecelakaan kerja
(karbon monoksida, pestisida, keracunan makanan, dll)

B. Mekanisme
Mekanisme cidera masing-masing racun memiliki efek patologis yang berbeda-
beda dimana masing masing racun memiliki patologi sendiri-sendiri. Efek racun
dapat terjadi pada tempat atau sekitar masuknya racun (misalnya reaksi kimia
sitotoksin) dan dapat berupa toksisitas sistemik yaitu efek-efek selektif racun atau
efek metabolik khusus dari racun itu terhadap target yang spesifik misalkan
asetaminofen di liver, methanol diretina, dll.

C. Pengkajian Prioritas Utama

1. Pengkajia riwayat kejadian, tanyakan pada pengantar pasien/pasien sendiri jika
kooperatif.
2. Pengjakian fisik : Initial assessment/ Arway- Breathing- Cirkulating ( ABC)
a. Tingkat kesadaran
b. Pernafasan dan efektifitas nafas
c. Irama jantung
d. Ada tidaknya kejang
e. Keadaan dan warna kulit
f. Besar dan reaksi pupil mata
g. lesi, bau mulut, dan lainnya
Terkadang setelah mendapatkan resusitasi (ABC) sering dilanjutkan dengan
perawatan suportif di ICU dan dilakukan pengeluaran zat penyebab dari tubuh
serta mungkin diperlukan antidotumnya.
Jika didapat pasien tidak sadar dengan penyebab yang Belum jelas, perlu selalu
difikirkan adanya kemungkinan intoksikasi. tindakan pertama:menjaga jalan
nafas, oksigen ( biasanya tidak kurang dari 6 lt / menit), K/p bantuan nafas, IV line,
kemudian cek seluruh tubuh adanya tanda-tanda kemungkinan mendapat obat
atau racun, periksa adanya bekas suntikan, zat terminum bau nafas dan lainnya
dan perkirakan juga kemungkinan terjadinya hipoglikemi.

D. Evaluasi/outcome umum pd intoksikasi

Stabilisasi & menigkatnya kardiorespirasi, kriteria :
sistolik 100mmHg, nadi 60 – 100X / menit, irama reguler
respirasi 24 X/ menit, tidak ada rales, tidak ada wheezing
meningkatnya kesadaran

1. Carbon Monoxide Poisoning

Carbon monoxide (CO), is a colorless, odorless, toxic gas that is a product of
incomplete combustion. Motor vehicles, heaters, appliances that use carbon
based fuels, and household fires are the main sources of this poison.
2. Carbon monoxide (CO)
Carbon monoxide (CO) intoxication is the leading cause of death due to poisoning
in the United States and also the most common cause of death in combustion
related inhalation injury. The incidence of non-lethal CO poisoning is not well
established nor is that of unrecognized CO poisonin. Mortality rates as high as
31% have been reported in large series
3. Agent
Most immediate deaths from building fires are due to CO poisoning and
therefore, fire fighters are at high risk.
a. Exogenous Sources of CO
b. Car exhaust fumes
c. Furnaces
d. Gas-powered engines
e. Home water heaters
f. Paint removers containing methylene chloride
g. Pool heaters
h. Smoke from all types of fire
i. Sterno fuel
j. Tobacco smoke
k. Wood stoves

E. Pathophysiology
In patients who die early following CO poisoning the brain is edematous, and
there are diffuse petechia and hemorrhages. If the victim survives initially but dies
within a few weeks, findings typical of ischemic anoxia are prominent.
Interestingly, the severity of the lesions appears to correlate best with the degree
of hypotension rather than with hypoxia.
1. Hypoxia and cellular asphyxia
CO combines preferentially with hemoglobin to produce COHb, displacing oxygen
and reducing systemic arterial oxygen (O2) content. CO binds reversibly to
hemoglobin with an affinity 200- 230 times that of oxygen. Consequently,
relatively minute concentrations of the gas in the environment can result in toxic
concentrations in human blood. Possible mechanisms of toxicity include: decrease
in the oxygen carrying capacity of blood. Alteration of the dissociation
characteristics of oxyhemoglobin, further decreasing oxygen delivery to the
tissues. Decrease in cellular respiration by binding with cytochrome a3. Binding to
myoglobin, potentially causing myocardial and skeletal muscle dysfunction.
2. Ischemia.
In addition to causing tissue hypoxia, CO can cause injury by impairing tissue
perfusion, indicate that myocardial depression, peripheral vasodilation, and
ventricular arrhythmia causing hypotension may be important in the genesis of
neurologic injury.
3. Reperfusion injury
Many of the pathophysiologic changes are similar to those seen with postischemic
reperfusion injuries, and similar pathology occurs in the brain in the absence of
CO when hypoxic hypoxia precedes an interval of ischemia.
F. Symptomatology
Many victims of CO poisoning die or suffer permanent, severe neurological injury
despite treatment. In addition, as many as 50% of those who recover
consciousness and survive may experience varying degree of more subtle but still
disabling neuropsychiatric sequela.
The features of acute CO poisoning are more dramatic than those resulting from
chronic exposure. The clinical presentation of acute CO poisoning is variable, but
in general, the severity of observed symptoms correlates roughly with the
observed level of COHb:
COHb Levels and Symptomatology
a. 10% Asymptomatic or may have headaches
b. 20% Dizzyness, nausea, and syncope
c. 30% Visual disturbances
d. 40% Confusion and syncope
e. 50% Seizures and coma
f. 60% Cardiopulmonary dysfunction & death

G. Management
The mainstay of therapy for CO poisoning is supplemental O2, ventilatory support
and monitoring for cardiac arrhythmias. There is general agreement that 100%
oxygen should be administered prior to laboratory confirmation when CO
poisoning is suspected. The goal of oxygen therapy is to improve the O2 content
of the blood by maximizing the fraction dissolved in plasma (PaO2).36 Once
treatment begins, O2 therapy and observation must continue long enough to
prevent delayed sequelae as carboxymyoglobin unloads.
The most controversial and widely debated topic regarding CO poisoning is the
use of hyperbaric oxygen (HBO). The most controversial and widely debated topic
regarding CO poisoning is the use of hyperbaric oxygen (HBO) severe poisoning
should be treated with 100% oxygen, with endotracheal intubation in patients
who cannot protect their airway. In these patients, consideration should be given
to transfusion of packed red blood cells.
H. Prognosis
30% of patients with severe poisoning have a fatal outcome.49 One study has
estimated that 11% of survivors have long-term neuropsychiatric deficits,
including 3% whose neurologic manifestations are delayed. One third of CO
poisoning victims may have subtle but lasting memory deficits or personality
changes.40. Indicators of a poor prognosis include altered consciousness at
presentation, advanced age, patients with underlying cardiovascular disease,
metabolic acidosis, and structural abnormalities on CT or MRI scanning.
Organophosphate and Carbamate Poisioning
Although OPC and carbamates are structurally distinct, they have similar clinical
manifestations and generally the same management. Although most patients with
OPC and carbamate poisoning have a good prognosis, severe poisoning is
potentially lethal. Early diagnosis and initiation of treatment are important. The
ED physician has access to a number of therapeutic options that can decrease
morbidity and mortality.

I. Pathophysiology
OPCs and carbamates bind to 1 of the active sites of acetylcholinesterase (AChE)
and inhibit the functionality of this enzyme by means of steric inhibition. The main
purpose of AChE is to hydrolyze acetylcholine (ACh) to choline and acetic acid.
Therefore, the inhibition of AChE causes an excess of ACh in synapses and
neuromuscular junctions, resulting in muscarinic and nicotinic symptoms and
signs.
Excess ACh in the synapse can lead to 3 sets of symptoms and signs. First,
accumulation of ACh at postganglionic muscarinic synapses lead to
parasympathetic activity of smooth muscle in lungs, the GI tract, heart, eyes,
bladder, and secretory glands, and increased activity in postganglionic
sympathetic receptors for sweat glands. This results in the symptoms and signs
that can be remembered with the mnemonic SLUDGE/BBB. Second, excessive ACh
at nicotinic motor end plates causes persistent depolarization of skeletal muscle
(analogous to that of succinylcholine), resulting in fasciculations, progressive
weakness, and hypotonicity. Third, as OPs cross the blood-brain barrier, they may
cause seizures, respiratory depression, and CNS depression for reasons not
completely understood.

J. Signs & Symptoms

Patients often present with evidence of a cholinergic toxic syndrome, or
toxidrome. SLUDGE/BBB mnemonic :
S = Salivation
L = Lacrimation
U = Urination
D = Defecation
G = GI symptoms
E = Emesis
B = Bronchorrhea
B = Bronchospasm
B = Bradycardia

DUMBELS mnemonic
D = Diarrhea and diaphoresis
U = Urination
M = Miosis
B = Bronchorrhea, bronchospasm, and bradycardia
E = Emesis
L = Lacrimation
S = Salivation

K. Lab & Test

Serum cholinesterase and RBC AChE activity, which are used to estimate neuronal
AChE activity. Other Tests: ECG, prolonged QTc interval is the most common ECG
abnormality. Elevation of the ST segment, sinus tachycardia, sinus bradycardia,
and complete heart block (rare) may also occur. (Sinus tachycardia occurs just as
commonly as sinus bradycardia.)

L. Prehospital Care
Identification of the type of chemical is important. As a general rule, dimethyl
OPCs undergo rapid aging, which makes early initiation of oximes critical. In
comparison, diethyl compounds may cause delayed toxicity, and oxime therapy
may need to be prolonged.
M. Emergency Department Care
1. ABC
Care of the ABCs should be initiated first because intubation may be necessary in
cases of severe poisoning. Because succinylcholine is metabolized by means of
plasma cholinesterase, OPC or carbamate poisoning may cause prolonged
paralysis. Increased doses of nondepolarizing agents, such as pancuronium or
vecuronium, may be required to achieve paralysis because of the excess ACh at
the receptor.
Providers with appropriate personal protective equipment (PPE) can address the
ABCs before decontamination atropine can precipitate ventricular fibrillation in
hypoxic patients. Paradoxically, the early use of adequate atropine will dry
respiratory secretions, improve muscle weakness and thereby improve
oxygenation. The following should be monitored on a regular basis to assess the
patient's respiratory status:
a. Respiratory rate
b. Tidal volume/ vital capacity
c. Neck muscle weakness
d. Ocular muscle involvement eg. diplopia
e. Arterial blood gas analysis
f. Cardiac monitoring, a wide range of cardiac manifestations can occur and
careful haemodynamic and electrocardiac monitoring hypoxaemia, metabolic and
electrolyte abnormalities can all contribute to cardiac arrhythmias. Some
arrhythmias may require cardiac pacing.
2. Decontamination:
Important part of the initial care, decontamination depends on the route of
poisoning. The patient's body should then be thoroughly washed with soap and
water to prevent further absorption from the skin. Washing the poisioned person
and removing contaminated clothes nosocomial poisoning in staff members
treating patients who have been exposed to OPCs and carbamates; the odors
often smelled when one cares for a patient poisoned from pesticide are
commonly due to the hydrocarbon solvent, which may cause symptoms
independent of the OPC agent. The patient's clothes must be removed and
isolated, and his or her body washed with soap and water.GI decontamination:
Oral administration of activated charcoal is a reasonable intervention after GI
poisoning. Gastric emptying should then be considered if the patient presents
within 1 hour of ingestion. Gastric lavage is the only means of emptying the
stomach in unconscious patients in which case the airway needs to be protected.
3. Atropine
Atropine is a pure muscarinic antagonist that competes with ACh at the
muscarinic receptor.
most commonly given in intravenous (IV) form at the recommended dose of 2-5
mg for adults and 0.05 mg/kg for kids with a minimum dose of 0.1 mg to prevent
reflex bradycardia. Atropine may be redosed every 5-10 minutes. Severe OP
poisonings often require hundreds of milligrams of atropine. In 1 case report, a
patient required frequent doses of atropine and was eventually converted to an
atropine infusion to a total of 30 g over 5 days.
Most sources recommend starting atropine on patients with anything more than
ocular effects and then observing the drying of secretions as an endpoint in
titrating to the appropriate dose. From the Tokyo sarin experience, patients
poisoned by nerve agents had modest atropine requirements, with none
requiring more than 10 mg. The recommended starting dose of atropine is a 2mg
IV bolus. Subsequent doses of 2-5mg every 5-15 minutes should be administered
until atropinization is achieved. The signs of adequate atropinization include an
increased heart rate (>100 beats/min.), moderately dilated pupils, a reduction in
bowel sounds, a dry mouth and a decrease in bronchial secretions.
4. Benzodiazepines
Seizures are an uncommon complication of OP poisoning. When they occur, they
represent severe toxicity.
5. Other treatments
magnesium and fresh-frozen plasma as adjunctive therapy. both must be
evaluated. Nebulized ipratropium bromide as an adjunct agent.

N. Management of Organophosphorus compunds poisoning

1. Skin decontamination **
2. Airway protection if indicated **
3. Gastric lavage
4. Activated charcoal 0.5-1gm/kg every 4hr
5. Anticholinesterase: Atropine/glycopyrrolate **
6. Cholinesterase reactivator: Pralidoxine
7. Ventilatory support
8. Inotropic support
9. Benzodazepines ( if seizure) **
10. Feeding-enteral/parental
** = useful

O. Further Inpatient Care

Patients who require continuous monitoring or treatment should be admitted to
the ICU. Patients with clinically significant poisoning should be evaluated
frequently to monitor their airway and respiratory secretions. In addition,
frequent neurologic examination should be performed to evaluate for
neuromuscular blockade. Therapy is largely titrated to the physical findings.
Atropinization is based on the drying of respiratory secretions, and oxime therapy
is based on an improvement in neuromuscular signs. A toxicologist may be of help
in determining specific aging and reactivation times of the particular OPC or
carbamate agent.

P. Further Outpatient Care:

Patients without any symptoms and with questionable or minimal exposure to
OPs or carbamates may be considered for discharge after 6-12 hours of
observation. Patients with residual neurologic symptoms should be given a
follow-up appointment with a neurologist. Follow-up with a psychiatrist should be
arranged as indicated.

Q. Complications
1. Intermediate syndrome, Intermediate syndrome was first described in 1987 as
a sudden respiratory paresis, with weakness in cranial nerves and proximal-limb
and neck flexor muscles. These clinical features appear 24-96 hours after
exposure and are distinct from the previously described delayed neurotoxicity
(see below). Although intermediate syndrome is incompletely understood, more
recent reports suggest this is due to presynaptic and postsynaptic dysfunction of
neuromuscular transmission and that it may result from insufficient oxime
treatment.
2. OPC-induced delayed neurotoxicity (OPCIDN), OPCIDN is a sensorimotor
polyneuropathy that typically occurs 9-14 days after OP exposure. The patient
initially presents with distal motor weakness and sensory paresthesias in the
lower extremities, which may progress proximally and eventually affect the upper
extremities. Most sources suggest the mechanism involves inhibition of
neuropathy target esterase (NTE), an enzyme that metabolizes esters in nerve
cells. Some patients may recover over 12-15 months, but permanent losses with
spasticity and persistent upper motor neuron findings have been reported.
3. Pancreatitis, Pancreatitis has been reported as a rare complication. One case
series reported that 12.76% of OP poisonings were associated with acute
pancreatitis, though this has not been the experience in other series.

R. Prognosis
In severe poisoning, death usually occurs within the first 24 hours if it is
untreated. With nerve-agent poisoning, death may occur within minutes if
untreated. Even with adequate respiratory support, intensive care, and specific
treatment with atropine and oximes, the mortality rate is still high in severe
poisonings. A delay in treatment can also lead to late and permanent neurologic
sequelae. Most patients with minimal symptoms fully recover.

S. Special Concerns
Pregnant women should receive the same treatment as that given to other adults.
Both atropine and pralidoxime are class C drugs in pregnancy. In the Tokyo
subway attacks, 5 pregnant women were mildly poisoned, and all had normal
babies without complications.