drms
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Gtreat Angel 
Best of luck
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| angel23
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TOXICOLOGY GENERAL PRINCIPLES
1. induced vomiting:ipecac....useful only if givn within 1-2 hrs
ipecac can delay the use of oral antidotes(charcoal n N acetylcysteine)
2.lavage :should be done with altered mental status where ipecac is C/I
useful only if given in first hour
BOTH IPECAC AND LAVAGE C/I WITH CAUSTIC SUBS.INGESTION
3.charcoal :if pt arrives after 1-2 hrs
charcoal not effective for hydrocarbons(methanol,ethylene glycol) and for metals such as iron
4.whole bowel ingestion
for large volume pill seen on Xray
polyethylene glycol(GoLYTELY)is adminstered
5.dialysis
done in coma,hypotension /apnoea
haemodialysis>>>>>peritoneal dialysis
6.cathartics:used only with charcoal
7.forced diuresis
done only in salicyalates and phenobarbital ingestion
8.naloxone/dextrose/thiamine
altered mental status + coma
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| angel23
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thanks drms
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| angel23
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Topics: 42
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ACETAMINOPHEN TOXICITY
The toxic dose of APAP after a single acute ingestion is 150 mg/kg or approximately 7 g in adults
History
The course of acetaminophen toxicity generally is divided into 4 phases. Clinical evidence of end-organ (hepatic, renal) toxicity is often delayed 24-48 hours postingestion.
Because antidotal therapy is most effective when initiated within 8 hours postingestion, the clinician must obtain an accurate history of the time(s) of ingestion, the quantity, and formulation of acetaminophen ingested, and any co-ingestants, which may delay APAP absorption (eg, anticholinergic drugs or opioids).
Because a patient's history may be inaccurate, the serum acetaminophen concentration is important for diagnosis and treatment, even in the absence of symptoms. After a single ingestion, NAC therapy is guided by the serum APAP concentration.
Phase 1 (0-24 h)
Asymptomatic
Anorexia
Nausea or vomiting
Malaise
Subclinical rise in serum transaminases levels begins at about 12 hours postingestion
Phase 2 (18-72 h)
Right upper quadrant abdominal pain, anorexia, nausea, vomiting
Continued rise in serum transaminases levels
Phase 3 (72-96 h)
Centrilobular hepatic necrosis with continued abdominal pain
Jaundice
Coagulopathy
Hepatic encephalopathy
Nausea and vomiting
Renal failure
Fatality
Phase 4 (4 d to 3 wk)
Complete resolution of symptoms
Complete resolution of organ failure
Physical
Physical examination findings vary, depending on the phase of toxicity.
Phase 1
Pallor
Malaise
Vomiting
Diaphoresis
Phase 2
Right upper quadrant abdominal tenderness
Tachycardia
Hypotension
Phase 3
Tender hepatic edge
Jaundice
Evidence of coagulopathy, including gastrointestinal (GI) bleeding
Evidence of hepatic encephalopathy
Phase 4: Resolution
Lab Studies
Acetaminophen serum concentration
A serum acetaminophen concentration drawn 4 or more hours after a single ingestion may be plotted on the Rumack-Matthew nomogram as a guide to recommended NAC therapy. The nomogram is not applicable after multiple or chronic ingestions. It may be less reliable following ingestions that include anticholinergics or opioids or extended-release formulations
Aspartate aminotransferase (AST) and alanine aminotransferase (ALT) begin to rise within 24 hours postingestion and peak at about 72 hours.
AST >> ALT
Toxicity is defined as serum AST or ALT levels greater than 1000 IU/L.
Rx
gastric emptying
activated charcoal
NAC given in all cases within 24 hrs of ingestion although most efficaccious when given within 8-10 hrs
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| angel23
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METHANOL :visual disturbance
ETHYLENE GLYCOL :renal failure ,oxalate crystals,hypocalcemia
both involve elevated anion gap acidosis
ISPROPYL ALCOHOL ingestion:ketosis without elevated anion gap acidosis
Rx
ethanol infusion followed by hemodialysis
fomipezole
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| angel23
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CO POISONING
History
Misdiagnosis commonly occurs because of the vagueness and broad spectrum of complaints; symptoms often are attributed to a viral illness. Specifically inquiring about possible exposures when considering the diagnosis is important. Any of the following should alert suspicion in the winter months, especially in relation to the previously named sources and when more than one patient in a group or household presents with similar complaints. Symptoms may not correlate well with HbCO levels.
Acute poisoning
Malaise, flulike symptoms, fatigue
Dyspnea on exertion
Chest pain, palpitations
Lethargy
Confusion
Depression
Impulsiveness
Distractibility
Hallucination, confabulation
Agitation
Nausea, vomiting, diarrhea
Abdominal pain
Headache, drowsiness
Dizziness, weakness, confusion
Visual disturbance, syncope, seizure
Fecal and urinary incontinence
Memory and gait disturbances
Bizarre neurologic symptoms, coma
Chronic exposures also present with the above symptoms; however, they may present with loss of dentation, gradual-onset neuropsychiatric symptoms, or, simply, recent impairment of cognitive ability.
Physical
Physical examination is of limited value. Inhalation injury or burns should always alert the clinician to the possibility of CO exposure.
Vital signs
Tachycardia
Hypertension or hypotension
Hyperthermia
Marked tachypnea (rare; severe intoxication often associated with mild or no tachypnea)
Skin: Classic cherry red skin is rare (ie, "When you're cherry red, you're dead"); pallor is present more often.
Ophthalmologic
Flame-shaped retinal hemorrhages
Bright red retinal veins (a sensitive early sign)
Papilledema
Homonymous hemianopsia
Noncardiogenic pulmonary edema
Neurologic and/or neuropsychiatric
Patients display memory disturbance (most common), including retrograde and anterograde amnesia with amnestic confabulatory states.
Patients may experience emotional lability, impaired judgment, and decreased cognitive ability.
Other signs include stupor, coma, gait disturbance, movement disorders, and rigidity.
Patients display brisk reflexes, apraxia, agnosia, tic disorders, hearing and vestibular dysfunction, blindness, and psychosis.
Long-term exposures or severe acute exposures frequently result in long-term neuropsychiatric sequelae. Additionally, some individuals develop delayed neuropsychiatric symptoms, often after severe intoxications associated with coma.
After recovery from the initial incident, patients present several days to weeks later with neuropsychiatric symptoms such as those just described. Two thirds of patients eventually recover completely.
MRI changes may remain long after clinical recovery. Predicting and preventing long-term complications and delayed encephalopathy have been the object of recent studies, many of which focus on the role of hyperbaric oxygen therapy.
lab:
<10% smokers
20-30% mild Sx
30-50% mod.Sx
>50-60% may be fatal
CPK may be elevated
metabolic acidosis
Rx...
removal from source
100%oxygen administration
hyperbaric oxygen in severe cases
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| angel23
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CAUSTIC TOXICITY
alkaline ingestion produces liquefactive necrosis and acid produces coagulative necrosis
alkali exposures more serious than acid exposures
History: The identity, concentration, pH or pKa, and amount of substance ingested are important. The time, nature of exposure, duration of contact, and any immediate on-scene treatment are important in determining management of toxicity.
Dyspnea
Dysphagia
Oral pain and odynophagia
Chest pain
Abdominal pain
Nausea and vomiting
Physical:
Impending airway obstruction
Stridor
Hoarseness
Dysphonia or aphonia
Respiratory distress, tachypnea, hyperpnea
Oropharyngeal burns: Significant esophageal involvement may occur without the presence of oropharyngeal lesions.
Drooling
Subcutaneous air
Acute peritonitis
Abdominal guarding
Rebound tenderness
Diminished bowel sounds
Hematemesis
Physical examination findings may be deceptively unremarkable after a significant acid ingestion, despite the presence of significant tissue necrosis.
Rx
immediately wash mouth with cold water
irrigate eye...see with flourescein for abrasions
donot induce emesis
just give water
donot give acid/base to neutralise....produces heat rxn
charcoal not useful
steroids C/I in perforation
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| angel23
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DIGOXIN TOXICITY
History
Constitutional symptoms (eg, weakness, fatigue)
Cardiovascular
Palpitations
Syncope
Dyspnea
Central nervous system
Confusion and somnolence
Dizziness without vertigo
Agitation, delirium, and hallucinations
Headache
Paresthesias and neuropathic pain
Seizures (extremely rare)
Ocular
Disturbances of color vision with a tendency to yellow-green coloring
Blurred vision and diplopia
Halos and scotomas
Photophobia
Gastrointestinal
Nausea, vomiting, anorexia, and diarrhea
Abdominal pain (uncommon)
Physical
Hemodynamic instability is related directly to the presence of a dysrhythmia or acute congestive heart failure (CHF).
Cardiovascular findings on physical examination relate to the severity of CHF, dysrhythmias, or hemodynamic instability.
Digoxin toxicity may cause any dysrhythmia. Classically, dysrhythmias that are associated with increased automaticity and decreased AV conduction occur (ie, paroxysmal atrial tachycardia with 2:1 block, accelerated junctional rhythm, or bidirectional ventricular tachycardia [torsade de pointes]).
Premature ventricular contractions (PVCs) are the most common dysrhythmia. Bigeminy or trigeminy occurs frequently.
Sinus bradycardia and other bradyarrhythmias are very common. Slow atrial fibrillation with very little variation in the ventricular rate (regularization of the R-R interval) may occur.
First- and second-degree AV block, complete AV dissociation, and third-degree heart block are also very common.
Rapid atrial fibrillation or atrial flutter is rare.
Ventricular tachycardia is an especially serious finding.
Cardiac arrest from asystole or ventricular fibrillation is usually fatal.
Gastrointestinal symptoms are common, but the abdominal examination is usually nonspecific.
Neurological findings are related to changes in sensorium or mental status. Lateralizing findings usually indicate another disease process.
Visual changes occur, but the pupils are spared, and objective findings are few.
Drug-induced fever does not occur.
Hypokalemia, hypernatremia, or hypomagnesemia increases the toxic cardiovascular effects of digoxin because of their depressive effects on the NA+/K+ ATPase pump.
Digoxin toxicity does not cause hypokalemia, but hypokalemia can worsen digoxin toxicity.
Hyperkalemia is the usual electrolyte abnormality precipitated by digoxin toxicity, primarily in the acute setting. Hyperkalemia may be associated with acute renal failure that subsequently precipitates digoxin toxicity.
PAT most common arythmias
Rx
Initiate supportive therapy with oxygen, cardiac monitoring, and IV access.
Activated charcoal is indicated for acute overdose or accidental ingestion. Cholestyramine binds enterohepatically-recycled digoxin and digitoxin, although no outcome studies have been performed.
Gastric lavage increases vagal tone and may precipitate or worsen arrhythmias. Consider pretreatment with atropine if gastric lavage is performed.
The availability of a digitalis-fab antibodies (Digibind) antidote usually renders gastric lavage unnecessary.
Management of dysrhythmias varies, depending on the presence or absence of hemodynamic instability, the nature of the arrhythmia, the presence or absence of electrolyte disturbances, and the preferences of toxicology and/or cardiology consultants.
Bradyarrhythmias that are hemodynamically stable may be treated with observation and discontinuation of the drug. Ensure proper hydration to optimize renal clearance of excess drug. GI binding agents (eg, charcoal, cholestyramine) may be utilized to bind enterohepatically-recycled digitalis.
Hemodynamically stable supraventricular arrhythmias may be treated conservatively with observation and discontinuation of digoxin. In the setting of rate-related ischemia or hemodynamic instability, Digibind is the treatment of choice.
Hemodynamically unstable bradyarrhythmias respond best to Digibind. Atropine may be used for temporary adjuncts. Cardiac pacing has been used successfully, but it can lower the fibrillatory threshold and induce arrhythmias.
PVCs, bigeminy, or trigeminy may be observed unless the patient is hemodynamically unstable, in which case lidocaine may be effective.
Ventricular tachycardia responds best to Digibind. Lidocaine and Dilantin may be useful. Lidocaine may be given in boluses of 100 mg, according to advanced cardiac life support (ACLS) guidelines. If lidocaine is successful, begin a maintenance infusion at 1-4 mg/min. Phenytoin has been administered in boluses of 100 mg every 5-10 min up to a loading dose of 15 mg/kg. Avoid procainamide and bretylium.
Asystole and ventricular fibrillation are very serious findings. Digibind is indicated; however, its effect is limited by poor cardiac blood flow. Nevertheless, the use of digoxin-fab fragments is associated with a 50% survival rate.
Cardioversion is relatively contraindicated because asystole or ventricular fibrillation may be precipitated.
Calcium channel blockers are contraindicated because they may increase digoxin levels.
Short-acting beta-blockers (eg, esmolol) may be helpful, but advanced or complete AV block may be precipitated.
Consider magnesium therapy as a temporizing antiarrhythmic agent until fab fragments are available. It may be lifesaving when ventricular tachycardia or ventricular fibrillation is present.
After an initial bolus of 2 g intravenously, a maintenance infusion at 1-2 g/h is initiated.
Monitor magnesium levels approximately every 2 hours. The therapeutic goal is a level between 4 and 5 mEq/L.
Correct electrolyte abnormalities, especially hypokalemia and hypomagnesemia. Dysrhythmias may be reversed with correction of electrolyte imbalances.
Treat hyperkalemia when K+ level is greater than 5.5 mEq/L.
Calcium is not recommended to treat hyperkalemia in this setting because ventricular tachycardia or ventricular fibrillation may be precipitated. This is based on the fact that intracellular calcium levels are already high in the setting of digoxin toxicity. However, anecdotal case reports and animal studies have been published that refute the dangers of calcium administration. Unless the patient is in extremis, other measures should be preferentially used to treat hyperkalemia.
Sodium bicarbonate and/or glucose and insulin are indicated.
Treatment with digoxin-fab fragments is indicated for hyperkalemia with K+ level greater than 5 mEq/L.
Kayexalate (0.5 g/kg PO) also is helpful in binding potassium and enterohepatically-recycled digitalis. However, digoxin-induced hyperkalemia reflects an extracellular shift, not an increase in total body potassium.
Caution is indicated when using Kayexalate concurrently with insulin/glucose/bicarbonate and/or Digibind because hypokalemia may be precipitated, which may worsen clinical toxicity.
Digoxin-fab fragments (Digibind) are generally indicated for the following:
Dysrhythmias associated with hemodynamic instability.
Altered mental status attributed to digoxin toxicity.
Hyperkalemia with K+ greater than 5 mEq/L.
Serum digoxin level greater than 10 ng/mL in adults at steady state (ie, 6-8 h post acute ingestion or at baseline in the clinical setting of chronic toxicity).
Ingestion greater than 10 mg in adults (40 X 0.25 mg tablets) or greater than 0.3 mg/kg in children
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| angel23
Forum Guru
Topics: 42
Posts: 980
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INH POISONING
antidote pyridoxine
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| angel23
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Topics: 42
Posts: 980
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OPC POISONING
Rx atropine
oximes(undergo aging)
BZP's for seizures
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| angel23
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Topics: 42
Posts: 980
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LEAD TOXICITY
Clinical findings
Neurological
Learning disability
Decreased IQ
Mental retardation
Encephalopathy
Motor deficits
Seizures
Cerebral edema
Hearing loss
Gastrointestinal
Abdominal pain
Nausea
Vomiting
Diarrhea
Constipation
Anorexia
Metallic taste in mouth
Ileus
Renal
Tubular damage
Azotemia
Gout
Hematologic
Affects blood synthesis
Hemolysis
RBC stippling
Iron deficiency
Musculoskeletal
Muscle and joint pain
Soft tissue
Blue-black line in gum margins
Endocrine
Decreased stature
Decreased growth hormone
Decreased vitamin D levels
Laboratory findings
Predate bone changes on x-ray
Serum Lead Level >1.2 umol/L
Urine lead level elevated
Peripheral Smear
Stippled erythrocytes
Complete Blood Count
Microcytic Anemia
Leukocytosis
Urine microscopy of sediment or renal biopsy
Acid-fast inclusion bodies in tubular nuclei
Pathognomonic for lead poisoning
Free Erythrocyte Protoporphyrin (FEP) > 0.6 umol/L
Imaging findings
Cerebral edema in acute lead intoxication
Particles of lead in GI tract
Bands of increased density at metaphyses of tubular bones (growing bone)
Metaphyses of growing bones may be dense normally
Lead lines more apt to be seen in proximal fibula and distal ulna where growth is not as great as other long bones
Lead lines may persist
Bone-in-bone appearance
Abnormalities in bone modeling
Erlenmeyer flask appearance to distal femur
Treatment
Surgical removal of lead foreign bodies in the gut (e.g. dice containing lead) if not eliminated within 2 weeks
Chelation is indicated if the level is greater than 45 mcg/dL even if asymptomatic
First correct iron deficiency
Chelating agents include EDTA, BAL, D-Penicillamine, and Succimer (used in children)
Attached Files:
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| angel23
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Topics: 42
Posts: 980
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MERCURY
interstitial pneumonitis
CNS Sx irreversible....erethism
Erethism is the constellation of irritability, excitability, anxiety, insomnia, and social withdrawal
GI Sx N/V pain
Rx
dimercaprol,succimer,penicillamine
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| angel23
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Topics: 42
Posts: 980
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SALICYLATES
Physical
Pulmonary
Hyperventilation (common)
Hyperpnea
Noncardiogenic pulmonary edema
Respiratory arrest
Apnea
Aspiration pneumonitis
Auditory
Ototoxicity
Tinnitus
Tinnitus is commonly encountered when serum salicylate concentrations exceed 30 mg/dL.
Tinnitus is a nonspecific nonsensitive clinical effect of salicylism.
Deafness
Cardiovascular
Tachycardia, generally with minimal hemodynamic or clinical significance
Hypotension
Dysrhythmias (eg, ventricular tachycardia, ventricular fibrillation, multiple PVCs)
Asystole (with severe intoxication)
Electrocardiogram (ECG) abnormalities (eg, U waves, flattened T waves, QT prolongation), may reflect hypokalemia
Sudden hemodynamic deterioration secondary to respiratory depression
Respiratory depression limits the respiratory alkalosis and causes an increase in the nonionized portion of salicylate.
The nonionized fraction enters the tissues, especially the CNS.
Neurologic
CNS depression, with manifestations ranging from somnolence and lethargy to seizures and coma
Tremor
Blurring of vision
Seizures
Encephalopathy
Encephalopathic changes may include irritability, confusion, hyperactivity, and hallucinations
These clinical effects are usually associated with severe cases.
Cerebral edema (with severe intoxication)
Gastrointestinal
Nausea and vomiting, common
Epigastric pain
GI hemorrhage -Most common with chronic intoxication
Intestinal perforation
Pancreatitis
Hepatitis (generally in chronic toxicity, rare in acute toxicity)
Genitourinary
Acute renal failure is an uncommon complication of salicylate toxicity.
Renal failure may be secondary to multisystem organ failure.
Case reports have documented the presence of albuminuria.
Hematologic
Hematologic effects may include prolongation of the prothrombin and bleeding times and decreased platelet adhesiveness.
Disseminated intravascular coagulation (DIC) may be noted with multisystem organ failure in association with chronic salicylate toxicity.
Dermatologic
Contact dermatitis may develop from topical application.
Diaphoresis is a common sign in patients with salicylate toxicity.
Electrolytes
Dehydration
Hypokalemia may be a severe iatrogenic complication in patients treated with urinary alkalinization if sufficient potassium supplementation is not provided.
Hypocalcemia
Acidemia ...elevated anion gap metabolic acidosis
SIADH
in adults:acute :respiratory alkalosis
chronic:mixed alkalosis and met acidosis
in children only met acidosis
Rx
charcoal
alkalinisation of urine
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| ecfmg09
Forum Senior
Topics: 3
Posts: 262
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wow angel, good work and great journal. You are right on track. Way to go.
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| angel23
Forum Guru
Topics: 42
Posts: 980
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thanks ecfmg!!
how r u??
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| angel23
Forum Guru
Topics: 42
Posts: 980
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ok almost done with emegency med
so wud sign off now n wil do neuro tomorrow
will post more later
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| angel23
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Topics: 42
Posts: 980
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TCA TOXICITY
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| angel23
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Topics: 42
Posts: 980
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OTHER DRUG TOXICITY
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| angel23
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Topics: 42
Posts: 980
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HEAD TRAUMA
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