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7/30/2019 poisionet patien

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PEMICU 6_KGD

STEVANY M

405080070


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MANAGEMENT OF THE POISONED PATIENT

PRIMARY SURVEY

Firstpriorities

are ABCs

Airway should be cleared of vomitus or any other obstruction and an oral

airway or endotracheal tube inserted if needed.

For many patients, simple positioning in the lateral decubitus

position

Breathing observation and oximetry

if in doubt, by measuring arterial blood gases.

Patients with respiratory insufficiency should be intubated and

mechanically ventilated

Circulation should be assessed by continuous monitoring of pulse rate, blood

pressure, urinary output, and evaluation of peripheral perfusion.

An iv line should be placed and blood drawn for serum glucose

and other routine determinations.


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SECONDARY SURVEY

History & Physical Examination

Laboratory & Imaging Procedures

Toxicology Screening Tests Decontamination

Specific Antidotes

Methods of Enhancing Elimination of Toxins


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FIGURE 1: ASSESSMENT AND MANAGEMENT OF THE POISONED PATIENT


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History & Physical Examination

Laboratory & Imaging Procedures

Toxicology Screening Tests Decontamination

Specific Antidotes

Methods of Enhancing Elimination of Toxins


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History

Need to obtain as much info as possible about

exposure

Number of exposed persons, type of exposure, amount or

dose, route Info from patient family, witness or EMT helpful

Check for empty bottles or containers, smells or unusual

containers, or suicide not


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PHYSICAL EXAMINATION

A brief examination should be performed, to

give clues to the toxicologic diagnosis.

These include :

vital signs, eyes and mouth, skin, abdomen, and

nervous system.


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Laboratory & Imaging ProceduresARTERIAL BLOOD GASES

Hypoventilation results in an elevated PCO2 (hypercapnia) and a low PO2

(hypoxia). The PO2

may also be low with aspiration pneumonia or drug-

induced pulmonary edema


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Decontamination


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Dissolve activated charcoal with water8-10 times

ACTIVATED CHARCOAL

0-1 YEAR 1g/kg

1- 12 year 20-25 g

>12 year 25-100g


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Methods of Enhancing Elimination of

Toxins

After appropriate diagnostic and decontamination

procedures and administration of antidotes, it is

important to consider whether measures forenhancing elimination, such as hemodialysis or

urinary alkalinization, can improve the clinical

outcome


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DIALYSIS PROCEDURES

there is two procedures :

1. peritoneal dialysis

2. hemodialysis

The efficiency of both peritoneal dialysis andhemodialysis is a function of the molecular

weight, water solubility, protein binding,endogenous clearance, and distribution in thebody of the specific toxin


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DIALYSIS PROCEDURES

Peritoneal Dialysis A relatively simple and available technique,

peritoneal dialysis is inefficient in removing

most drugs.


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DIALYSIS PROCEDURES

Hemodialysis

It assists in correction of fluid and electrolyte

imbalance and may also enhance removal of

toxic metabolites (eg, formic acid in methanol

poisoning; oxalic and glycolic acids in ethylene

glycol poisoning).


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DIALYSIS PROCEDURES

Hemodialysis is especially useful in overdose

cases in which the precipitating drug can be

removed and fluid and electrolyte imbalances

are present and can be corrected (eg,salicylate intoxication).


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Iron

Iron, which is essential to the function ofhemoglobin, myoglobin, many cytochromes,and many catalytic enzymes, can be extremely

toxic when levels are elevated following anoverdose.

The acute ingestion of iron is especiallyhazardous to children

Serious iron ingestions in adults are usuallyassociated with suicide attempts.


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Pathophysiology

Iron has two distinct toxic effects: It causes direct caustic injury to the

gastrointestinal mucosa

It impairs cellular metabolism, primarily of theheart, liver, and central nervous system (CNS).

The caustic effects of iron on the gutvomiting, diarrhea, and abdominal pain.

Hemorrhagic necrosis of gastric or intestinalmucosa bleeding, perforation, andperitonitis.


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Clinical Features

The clinical effects of acute iron

poisoning are described by five stages :

Phase I : reflects the corrosive effects ofiron on the gut. Vomiting occurs within 80

minutes of ingestion in more than 90% of

symptomatic cases. Diarrhea, which can be

bloody, follows


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Clinical Features

Phase II : represents an apparent (but not

complete) recovery that lasts less than 24

hours but can extend up to 2 days. Most

patients recover after this point.

Phase III : is characterized by the recurrence

of gastrointestinal symptoms, severe

lethargy or coma, anion gap metabolicacidosis, leukocytosis, coagulopathy, renal

failure, and cardiovascular collapse.


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Clinical Features

Phase IV : fulminant hepatic failure, occurs2 to 5 days after ingestion. This is relativelyrare, appears to be dose related, and is

usually fatal Phase V : represents the consequences of

healing the injured gastrointestinal mucosa.It is characterized by pyloric or proximal

bowel scarring, which is sometimesassociated with obstruction.


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Diagnostic


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Management

Iron is not bound to activated charcoal

Deferoxamine

The patient who has ingested more than 20

mg/kg of elemental iron, or has pills visible on

an abdominal radiograph, should receive

whole-bowel irrigation


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Lead

Lead poisoning is a disease of industrialization.

Exposure usually results from ingestion or

inhalation.

Ex: Household paint, curtain weights, buckshot,fishing weights, lead-contaminated soil or

water, food or beverages stored or prepared in

lead-soldered cans, lead-glazed pottery, andlead crystal decanters, toys


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Risk factor

Hobbies : making glazed pottery, target shooting

at indoor firing ranges, soldering lead, repairing

cars or boats, and remodeling homes.

Industries : lead smelting, battery manufacture,radiator repair, bridge and ship construction or

demolition, soldering or welding, cable or tin can

production, stained glass manufacture, glassproduction, firing range operation and lead-based

paint abatement.


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Clinical Features

cramping abdominal pain with nausea,

vomiting, constipation, and, occasionally,

diarrhea

Other characteristic symptoms and signs of

acute toxicity include fatigue, anemia,

peripheral neuropathy, renal impairment, and

hepatic and CNS dysfunction


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Clinical Features

The CNS toxicity may manifest as mild

headache or personality changes to fullblown

encephalopathy with coma, convulsions, and

papilledema.

Permanent neurologic and behavioral

sequelae may occur.


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Managemant

Chelation Therapy :

Any patient with a serum level greater than 70

g/dL, or with signs suggestive ofencephalopathy

parenteral chelation therapy. Dimercaprol [BAL] should be the first chelator

given

followed by calcium disodiumethylenediaminetetraacetic acid (CaNa2EDTA), a

highly effective lead chelator.


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Management

Patients who are significantly symptomatic

after an acute lead exposure and children with

a serum level of 69 g/dL or greater require

hospitalization and chelation therapy.

Patients discharged home on oral chelation

therapy should not return to a contaminated

environment.


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Arsenic

Arsenic (As), a tasteless, odorless substance that

looks like sugar, has an infamous history as an

agent of homicide.

It is used in industry as a wood preservative andin the production of glass and microcircuits.

Inorganic arsenicals are also used in rodenticides,

fungicides, insecticides, paint, and tanning agentsand as defoliants in the cotton industry


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Arsenic

It has also been found as a contaminant in

herbal remedies and drugs such as opium.

Arsenic is still used for medicinal purposes in

the treatment of trypanosomiasis, amebiasis,

and leukemia


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Clinical Features

Acute gastrointestinal effects nausea,

vomiting, abdominal pain, and diarrhea

(predominate as the initial manifestations of

acute exposure to arsenic salts).

These symptoms can be so severe as to result

in hematemesis and hematochezia.

Within 30 to 60 minutes of exposure, patientscomplain of a metallic or garlicky taste


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Clinical Features

In cases of severe poisoning, cardiovascular

collapse and death ensue

Less common complications include hepatitis,

rhabdomyolysis, hemolytic anemia, renal

failure, unilateral facial nerve palsy,

pancreatitis, pericarditis, pleuritis, and fetal

demise


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Diagnostic

Normal arsenic levels are 5 g/L or less in

blood or less than 50 g/day in a 24-hour

urine collection, which is the best way to

diagnose the poisoning.

Any urine level above 100 g/dayor 50 g/L

necessitates treatment

Radiograph Arsenic in the gastrointestinaltract is radiopaque


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Management

Hemodialysis removes arsenic in the setting of

acute renal failure.

Although there is no evidence for improved

outcomes, orogastric lavage or whole-bowel

irrigation should be considered only for very

recent (


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Management

Intramuscular dimercaprol is the preferred

chelator in patients who are critically ill

DMSA (Dimercaptosuccinic acid) is a water-

soluble analogue of dimercaprol that can be

given orally


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Mercury

Mercury is a silver white metal, familiar to

most as the only metal that is liquid at room

temperature


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Management

Gastric lavage with protein-containing

solutions (e.g., milk and egg whites) may be

beneficial in the decontamination of the

gastrointestinal tract following ingestion ofmercury sal

BAL is used for clinically significant acute

inorganic mercury intoxication.

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