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

0.5

1

1.5

2

713

月日

715

月日

717

月日

719

月日

725

月日

81

月日

88

月日

time

chol

ines

tera

se

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