2011.08.12指導醫師:許景瑋醫師報告者: fellow 1 陳筱惠
Name: 林 o 順Sex: maleAge: 69 years oldChart number: 2021918Date of admission: 2011/07/12
Ingestion of 陶斯松 about 350ml in the morning
69 year old man without significant systemic diseases
Ingestion of 陶斯松 about 350ml for suicide attempt on 7/12 morning
He vomited several times just after taking the agent. At 恩主公 hospital: NG gastric lavage with charchoal At ER:
Clear consiousness Associated symptoms?? wheezing, dyspnea, seizure,
lacrimation, sweating, diarrhea, abdominal pain, urine incontinence, muscle weakness
He was admitted to MICU-2.
He denied significant systemic diseases, such as diabetes mellutis , hypertension, heart, kidney, or lung diseases.
Operation history: for bilateral inguinal hernia years ago
Current medicine: nil
Allergy: no known allergyAlcohol: denied; betel-nut: denied;
cigarette: 1 ppd/day since young ageOver-the-counter medication or
chinese herb: denied
No family history of diabetes mellutis, malignancy, heart, liver, kidney, or hereditary diseases
Vital signs: blood pressure: 186/106mmHg; temperature: 35.8’C; pulse rate: 104/min; respiratory rate: 22/min
General apperance: acute ill looking Eye: pupil 3/3, conjunctiva: not pale, sclera: no icteric Neck: supple, no lymphadenopathy or jugular vein
engorgement Chest: symmetric expansion
breathing sound: bilateral clear, no wheezing or crackles
heart sound: regular heart beats, no S3 or S4, no
murmurs Abdomen: soft, not distended, no tenderness
liver/spleen: impalpable bowel sound: normoactive Extremities: no muscle weakness or lower limb pitting
edema Skin: intact, no rash
Organophosphate intoxication due to suicide attempt
Bilateral inguinal hernia post operation years ago
Give PAM for antidote (no Atropine??)
O2 support and IVF hydrationClosely monitor vital signs, clinical
condition, and respiratory patternCheck and rollow up plasma
cholinesterase level regularly
WBC 30.1x1000/ul
Hgb 13.1 g/dl
PLT 333 x1000/uL
Segment 84.0 %
Monocyte 8.5 %
Lymphocyte 7.5 %
Eosinophil 0.0 %
Basophil 0.0 %
Urea N 17.1 mg/dl
Creatinine 1.19 mg/dl
GPT 16 IU/L
NA 141 mEq/L
K 3.5 mEq/L
Amylase 167 IU/L
Cholinesterase 0.69 IU/ml
Troponin-I 0.031 ng/ml
CRP 13.85 mg/L
PAM
Atropine 2pc -> 4pc st for bronchorrhea/dyspnea
Intubation
Cefuroxime
Clindamycin
PAM
Extubation failure
Clindamycin
Cefuroxime Ceftazidime
PAM
Extubation
Ceftazidime
Transfer to Nephro ward
Ceftazidime
Atropine 1pc q12h
Ceftazidime
Atropine 1pc q12h
0.620.650.710.710.85
0.620.690.63
1.38
0.620.780.86
1.32
1.73
0
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1
1.5
2
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715
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chol
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Organophosphorous compounds bind to acetylcholinesterase (AChE) and render this enzyme non-functional AChE: the enzyme responsible for hydrolysis
of acetylcholine to choline and acetic acid After period of time, the
acetlycholinesterase-organophosphorous compound undergoes "aging," which renders the enzyme irreversibly resistant to reactivation by an antidotal oxime.
Carbamate compounds: transient cholinesterase inhibitors, which spontaneously hydrolyze from the cholinesterase enzymatic site within 48 hours Carbamate toxicity tends to be of shorter
duration than that caused by equivalent doses of organophosphates, although the mortality rates associated with exposure to these chemical classes are similar.
Onset and duration of AChE inhibition varies depending on Rate of AChE inhibition Route of absorption
▪ Oral or respiratory exposures: within 3 hours▪ Dermal absorption: 12 hours
Enzymatic conversion to active metabolites Lipophilicity
▪ Lipophilic agents are associated with delayed onset of symptoms (up to 5 days) and prolonged illness (greater than 30 days).
Cholinergic excess: autonomic nervous system, neuromuscular junction, and central nervous system (CNS)
SLUDGE/BBB : Salivation, Lacrimation, Urination, Defecation, Gastric Emesis, Bronchorrhea, Bronchospasm, Bradycardia
DUMBELS: Defecation, Urination, Miosis, Bronchorrhea/Bronchospasm/Bradycardia, Emesis, Lacrimation, Salivation
10~40%, 24~96hours Characteristic neurological findings:
neck flexion weakness, decreased deep tendon reflexes, cranial nerve abnormalities, proximal muscle weakness, and respiratory insufficiency
Risk factors: Highly fat-soluble organophosphorous agent
( 大滅松、芬殺松、亞素靈 ) Inadequate doses of oximes
1~3 weeks 達馬松、三氯松、美文松、陶斯松、巴拉松 Inhibition of neuropathy target esterase
(NTE) S/S:
Transient, painful "stocking-glove" paresthesias a symmetrical motor polyneuropathy (flaccid weakness of lower extremities, then ascends to upper extremities, primarily distal muscle)
Sensory disturbances: mild
EMG/NCV: decreased firing of motor conduction units
Histopathologic sections of peripheral nerves: Wallerian (or "dying-back") degeneration of large distal axons
Clinical features of cholinergic excess Petroleum or garlic-like odor Dimethyl or a diethyl compound??
Dimethyl compounds undergo rapid aging, making early initiation of oxime therapy critical. Diethyl compounds may exhibit delayed toxicity, and may require prolonged treatment.
A trial of 1 mg atropine in adults (or 0.01 to 0.02 mg/kg in children) The absence of signs or symptoms of
anticholinergic effects following atropine challenge strongly supports the diagnosis of poisoning with an acetylcholinesterase inhibitor.
Laboratory abnormalities : RBC acetylcholinesterase (RBC AChE):
Most hospital laboratories are unable to perform this test.▪ The degree of toxicity▪ The effectiveness of oxime therapy in
regeneration of the enzyme▪ Chronic or occupational exposure
Plasma (or pseudo-) cholinesterase
Early intubation: CNS respiratory center depression Nicotinic receptor mediated diaphragmatic
weakness, bronchospasm, and copious secretions
Avoid the use of succinylcholine when performing rapid sequence intubation (RSI) in patients with organophosphate (OP) poisoning Succinylcholine is metabolized by
acetylcholinesterase.
Adequate volume resuscitation with isotonic crystalloid (eg, normal saline or lactated Ringer's solution)
Decontamination: topical exposure We generally do not perform gastric
lavage.▪ Substantial risk of aspiration in patients with
increased secretions and decreased mental status
▪ Not decrease morbidity or mortality Patients presenting within 1 hour of an
organophosphorous agent or carbamate ingestion: activated charcoal 1 g/kg (max dose 50 g)
Forced emesis is contraindicated because of the risk of aspiration and seizures.
Urinary alkalinization has been suggested, but there is no clear evidence that this intervention improves outcome.
Atropine: Compete with acetylcholine at muscarinic
receptors; ineffective in treating neuromuscular dysfunction (nicotinic receptors)
A dose of 2 to 5 mg IV for adults and 0.05 mg/kg IV for children no effect, then bouble dose every 3~5 mins until pulmonary muscarinic S/S alleviating (clearing of respiratory secretions, cessation of bronchoconstriction) infusion of 10~20% of loading dose/hour
Atropine overdose
Pralidoxime: cholinesterase reactivating agents
Concurrent use of atropine to prevent worsening symptoms due to transient oxime-induced acetylcholinesterase inhibition
Dose: Adult Children
Bolus dose(slow ivf > 30 minutes, since rapid administration has occasionally been associated with cardiac arrest)
30 mg/kg 25~50 mg/kg
Continous dose 8mg/kg/hr 10 ~ 20 mg/kg/hr
Benzodiazepines: Organophosphorous agent-induced
seizures Prophylactic use has been shown to
decrease neurocognitive dysfunction after organophosphorous agent poisoning.
ABG
PH 6.856
PCO2 171.7 mmHG
PO2 121.3 mmHG
HCO3 29.7 mm/L
SaO2 93.7%
ABG
PH 7.202
PCO2 75.1 mmHG
PO2 115.4 mmHG
HCO3 36.5 mm/L
SaO2 97.0 %
7/13 blood culture: negative7/13 urine culture: negative7/15 sputum culture: Ps.aeruginosa
+ Kleb.pneumoniae