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PEMICU 6_KGD

STEVANY M 405080070

MANAGEMENT OF THE POISONED PATIENT


PRIMARY SURVEY First priorities 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.

SECONDARY SURVEY
History & Physical Examination Laboratory & Imaging Procedures Toxicology Screening Tests Decontamination Specific Antidotes Methods of Enhancing Elimination of Toxins

FIGURE 1: ASSESSMENT AND MANAGEMENT OF THE POISONED PATIENT

History & Physical Examination Laboratory & Imaging Procedures Toxicology Screening Tests Decontamination Specific Antidotes Methods of Enhancing Elimination of Toxins

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

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.

Laboratory & Imaging Procedures


ARTERIAL BLOOD GASES Hypoventilation results in an elevated PCO2 (hypercapnia) and a low PO2 (hypoxia). The PO2 may also be low with aspiration pneumonia or druginduced pulmonary edema

Decontamination

ACTIVATED CHARCOAL 0-1 YEAR 1- 12 year >12 year 1g/kg 20-25 g 25-100g

Dissolve activated charcoal with water 8-10 times

Methods of Enhancing Elimination of Toxins


After appropriate diagnostic and decontamination procedures and administration of antidotes, it is important to consider whether measures for enhancing elimination, such as hemodialysis or urinary alkalinization, can improve the clinical outcome

DIALYSIS PROCEDURES
there is two procedures : 1. peritoneal dialysis 2. hemodialysis The efficiency of both peritoneal dialysis and hemodialysis is a function of the molecular weight, water solubility, protein binding, endogenous clearance, and distribution in the body of the specific toxin

DIALYSIS PROCEDURES

Peritoneal Dialysis A relatively simple and available technique, peritoneal dialysis is inefficient in removing most drugs.

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).

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).

Iron
Iron, which is essential to the function of hemoglobin, myoglobin, many cytochromes, and many catalytic enzymes, can be extremely toxic when levels are elevated following an overdose. The acute ingestion of iron is especially hazardous to children Serious iron ingestions in adults are usually associated with suicide attempts.

Pathophysiology
Iron has two distinct toxic effects:
It causes direct caustic injury to the gastrointestinal mucosa It impairs cellular metabolism, primarily of the heart, liver, and central nervous system (CNS).

The caustic effects of iron on the gut vomiting, diarrhea, and abdominal pain. Hemorrhagic necrosis of gastric or intestinal mucosa bleeding, perforation, and peritonitis.

Clinical Features
The clinical effects of acute iron poisoning are described by five stages :
Phase I : reflects the corrosive effects of iron on the gut. Vomiting occurs within 80 minutes of ingestion in more than 90% of symptomatic cases. Diarrhea, which can be bloody, follows

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 metabolic acidosis, leukocytosis, coagulopathy, renal failure, and cardiovascular collapse.

Clinical Features
Phase IV : fulminant hepatic failure, occurs 2 to 5 days after ingestion. This is relatively rare, 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 sometimes associated with obstruction.

Diagnostic

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

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, and lead crystal decanters, toys

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, glass production, firing range operation and lead-based paint abatement.

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

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.

Managemant
Chelation Therapy :
Any patient with a serum level greater than 70 g/dL, or with signs suggestive of encephalopathy parenteral chelation therapy. Dimercaprol [BAL] should be the first chelator given followed by calcium disodium ethylenediaminetetraacetic acid (CaNa EDTA), 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.

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 and in the production of glass and microcircuits. Inorganic arsenicals are also used in rodenticides, fungicides, insecticides, paint, and tanning agents and as defoliants in the cotton industry

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

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, patients complain of a metallic or garlicky taste

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

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/day or 50 g/L necessitates treatment Radiograph Arsenic in the gastrointestinal tract is radiopaque

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 (<1 hr) ingestions or if radiopaque material is visualized on an abdominal radiograph.

Management
Intramuscular dimercaprol is the preferred chelator in patients who are critically ill DMSA (Dimercaptosuccinic acid) is a watersoluble analogue of dimercaprol that can be given orally

Mercury
Mercury is a silver white metal, familiar to most as the only metal that is liquid at room temperature

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 of mercury sal BAL is used for clinically significant acute inorganic mercury intoxication.