Dr.

Ali’s Uworld Notes For Step 2 CK

Poisoning
Torsades de points is a polymorphic ventricular tachycardia which occurs in the setting of a
prolonged QT interval and is seen in patients with familial long QT syndrome, malnourished
patients predisposed to hypomagnesemia (such as alcoholics), and in patients taking certain
drugs (tricyclic antidepressants), certain antiarrhythmics (amiodarone, sotalol), and anti-
infective agents (moxifloxacin, fluconazole). Treatment of torsades de points includes
cessation of any offending agents, and initiation of magnesium sulfate.

Beta Blockers OD - The combination of bradycardia, AV block, hypotension and diffuse

wheezing indicates overdose on beta-blockers. Intoxication of calcium channel blockers,
digoxin, and cholinergic agents would cause some of the above symptoms, but wheezing is
indicative of beta-blocker toxicity. The most common presentation of beta blocker toxicity is
bradycardia and hypotension, which can lead to cardiogenic shock, as indicated by cold and
clammy extremities in the patient. Other effects include bronchospasm (beta 2 blockade) as
evidenced by diffuse wheezing, neurological effects (delirium and seizures) and hypoglycemia.
To reverse the effects of toxicity, atropine and IV fluids are first given. If this fails to improve
blood pressure, glucagon is the next agent administered. Glucagon leads to an increase in
cAMP and higher levels of intracellular calcium, thereby augmenting cardiac contractility.

Diphenhydramine overdose leads to anti-histamine effects including drowsiness, confusion and

anticholinergic effects including dry mouth, dilated pupils, blurred vision, reduced bowel
sounds and urinary retention. Physostigmine, a cholinesterase inhibitor can counteract these
anti-cholinergic effects.

Acetaminophen Poisoning - The Rumack-Matthew nomogram provides the likelihood of

hepatotoxic effects from acetaminophen overdose and the need for N-acetylcysteine. The first
data point on the curve is at 4 hours. The decision of whether or not to administer the antidote
can be made after four hours, based on the acetaminophen level. As long as it is administered
within 8 hours of ingestion, the outcome will not be adversely affected. Besides, several
studies showed that there is no correlation between the amount of acetaminophen reportedly
taken and the measured serum drug level!

TCA Poisoning – TCA overdose causes hyperthermia, seizures, and hypotension as well as
anticholinergic effects including dilated pupils, flushed and dry skin, and intestinal ileus. TCA
overdose decreases myocardial conduction velocity, leading to QRS prolongation and risk of
developing ventricular arrhythmia. The EKG, with specific attention to the QRS complex, is the
best indicator of the extent of overdose because QRS duration has been shown in studies to
have value in predicting the likelihood of seizures and ventricular arrhythmia. Sodium
bicarbonate is used to treat TCA poisoning; it narrows the QRS complex and decreases the
incidence of ventricular arrhythmia.

Among the many significant cellular effects of tricyclic antidepressants, the inhibition of cardiac
fast sodium channels is responsible for QRS prolongation. QRS prolongation can lead to
ventricular arrhythmias and thus, narrowing of the QRS interval is a critical aspect of treatment
in TCA intoxication. In patients with a QRS interval of greater than 0.10 seconds, the physician
should administer sodium bicarbonate. Sodium bicarbonate reverses the prolongation of the
QRS interval by increasing the extracellular sodium concentration, besides, alkalinization of the
serum decreases drug avidity for the sodium channels.

Ethanol Poisoning -. Ethylene glycol and methanol poisoning occur when ingested as a
substitute for ethanol. The initial symptoms of ingestion of these poisons can mimic ethanol
inebriation. However, as alcohol dehydrogenase (ADH) metabolizes ethylene glycol to oxalic
acid and glycolic acid, these metabolites cause profound clinical consequences. Glycolic acid
injures the renal tubules, while oxalic acid binds calcium, causing hypocalcemia and calcium
oxalate crystal deposition in the kidneys. Once this occurs, patients develop flank pain,
hematuria, oliguria, acute renal failure and anion gap metabolic acidosis. All of these symptoms
are demonstrated in this case. Administration of either fomepizole or ethanol to achieve ADH
inhibition is an integral part of treatment. This prevents further breakdown of ethylene glycol
into its toxic metabolites.

Benzodiazepine Poisoning - A patient with benzodiazepine overdose presents with slurred

speech, unsteady gait, and drowsiness. Benzodiazepines are used for the treatment of anxiety,
insomnia, seizures and alcohol withdrawal. During benzodiazepine intoxication, pupil size tends
to be normal, with only mild respiratory depression.

Carbon Monoxide Poisoning - Carbon monoxide is a colorless, odorless gas emitted by

automobiles, furnaces and charcoal grills. When inhaled, it prevents the body's tissues from
utilizing oxygen effectively. Acute exposure can present with headaches, nausea, vomiting,
abdominal discomfort, confusion and coma. Patients often present with a pinkish-red skin hue.
Diagnosis is established by obtaining carboxyhemoglobin levels. Treatment consists of
hyperbaric oxygen administration.

Organophosphate Poisoning - Acetylcholinesterase is rendered non-functional in OP

poisoning, leading to symptoms of cholinergic excess. The common presentation includes
bradycardia, miosis, bronchorrhea, muscle fasciculations, salivation, lacrimation, diarrhea and
urination. To counteract the effects of organophosphate poisoning, atropine should be
administered immediately. It acts by competing with acetylcholine at the muscarinic receptors,
and would therefore reverse the patient's symptoms. Of equal importance is the immediate
removal of the patient's clothing (if soaked with vomitus) to prevent continued absorption of
organophosphates through the skin

Lye or Alkali Ingestion - Caustic poisoning does not cause alteration in consciousness. So the
patient will be alert & conscious, but in severe pain. It presents with dysphagia, severe pain,
heavy salivation and mouth burns (white tongue). The damage is the result of necrosis of the
tissue that lines the gastrointestinal tract. In severe cases, perforation of the stomach or
esophagus can occur, causing peritonitis or mediastinitis. Esophageal damage induced by lye
ingestion begins almost instantaneously. Alkaline solutions cause liquefactive necrosis of the
esophageal wall, which can lead to perforation and mediastinitis. Patients often present with
retrosternal/ epigastric pain, hypersalivation and odynophagia/dysphagia. Patients should be
hospitalized, given intravenous hydration, and receive serial abdominal and chest x-rays.
Endoscopy should be performed expeditiously to assess the extent of esophageal injury and to
determine if any further management is needed, If perforation is suspected, a Gastrografin
study should be performed.

Gastric decontamination with ipecac in patients with lye ingestion is contraindicated. The
damage caused by lye is instantaneous and inducing vomiting will only re-expose the esophagus
to lye, causing further injury.

Activated charcoal, when given within one hour of poison ingestion, has been shown to
improve outcomes for many types of toxic ingestions by decreasing the absorption of the
poison. However, damage caused by lye is immediate, and therefore decreasing absorption has
no role in treatment.

Neutralization of the alkali with a weak acid will not reverse the immediate damage caused by
the lye. Instead, the neutralization reaction can actually exacerbate injury by releasing heat.

Phencyclidine Abuse - phencyclidine, a commonly abused street drug which causes

hallucinations, dissociative feelings, agitation, confusion, pupillary dilation, tachycardia, and
nystagmus. It is the only illicit drug that causes vertical nystagmus, but horizontal and rotatory
nystagmus can also occur. In many cases, it can lead to psychotic and violent behavior. High
doses can cause severe hypertension, seizures, and life-threatening hyperthermia.
Benzodiazepines are used for treatment of severe psychomotor agitation.

Marijuana Abuse - Signs of marijuana use/intoxication include increased appetite, tachycardia,

tachypnea, hypertension, dry mouth, and conjunctival injection. Marijuana use decreases
reaction time and impairs attention, concentration and short-term memory. Impairment of
cognition, judgment, and coordination can last much longer than the acute euphoric effect,
affecting the ability to operate automobiles and increasing the risk of motor vehicle
accidents.

Opioid Intoxication - Opioid intoxication presents with miosis, depressed mental status,
decreased respiratory rate, decreased bowel sounds, hypotension and bradycardia. Of these,
decreased respiratory rate is the best predictor of intoxication and is also a frequent cause of
mortality. An important part of treatment for this patient is to administer naloxone, with the
goal of increasing his respiratory rate from 6/min to 12/min or greater and improving his
oxygen saturation.

Opioid Withdrawal - Patients with a history of opioid dependence typically develop withdrawal
within 6-12 hours after the last dose of short-acting Opioid, with a peak at 24-48 hours after
symptom onset. Symptoms of opioid withdrawal include nausea, vomiting, cramps, diarrhea,
dysphoria, restlessness, rhinorrhea, lacrimation, myalgias and arthralgias. Physical
examination can show mydriasis, piloerection and hyperactive bowel sounds. Although the
withdrawal symptoms caused by natural opioid cessation are not life-threatenin,. they can be
quite uncomfortable.

Methadone, either oral or intramuscular, is the treatment of choice to relieve withdrawal

symptoms in opioid-dependent patients & also for long term management. Methadone
replacement therapy for chronic management of addiction in the outpatient setting should not
be confused with therapy in the inpatient setting as the protocols used in these venues are
different.

Under federal law, the Drug Enforcement Agency permits treatment or prevention of opioid
withdrawal with methadone without regulatory restriction provided the treatment is inpatient
and the primary disease is medical (ie. not opioid withdrawal).

Alcohol Withdrawal - In any hospitalized patient with a suspected history of alcoholism,

precautions should be taken to prevent the symptoms of alcohol withdrawal. Symptoms of
alcohol withdrawal are the result of alcohol's CNS depressant effects. When alcohol is abruptly
discontinued, it leads to reflex hyperactivity in certain parts of the brain and manifests as
anxiety, insomnia, tremors, and diaphoresis in the first 6-24 hours after alcohol cessation.

Hallucinations and withdrawal seizures can also occur in the first 48 hours in these patients.
The most serious effect of alcohol withdrawal is delirium tremens, which occurs in 5% of
untreated patients. Delirium tremens occurs after 48- 96 hours, and consists of hypertension,
agitation, tachycardia, hallucinations, and fever, with a mortality rate of up to 5%. Due to the
serious potential complications of alcohol withdrawal, the patient should be placed in a
protective environment, and be treated with benzodiazepines, which are CNS depressants that
will limit the effects of alcohol withdrawal. Chlordiazepoxide (Librium) is a benzodiazepine and
a common choice of treatment for alcohol withdrawal.

Antipsychotic Induced Hypothermia - Fluphenazine is a "typical" antipsychotic medication that

is commonly injected every 2-3 weeks in schizophrenics with poor compliance. More potent
than haloperidol, fluphenazine can cause hypothermia by inhibiting the body's shivering
mechanism and/or inhibiting autonomic thermoregulation. For this reason, patients taking
antipsychotic medications should be advised to avoid prolonged exposure to cold
temperatures. Under such conditions, they can develop extreme hypothermia.

Neuroleptic Malignant Syndrome - The combination of recent onset confusion, fever, muscle
rigidity and diaphoresis are consistent with the diagnosis of Neuroleptic Malignant Syndrome
(NMS), a drug induced idiosyncratic reaction. These patients have a history of psychosis or
hallucinations and are most likely on a dopaminergic antagonist medication, such as
haloperidol. The "typical" neuroleptic agents (such as haloperidol) are most frequently
implicated in NMS but other dopaminergic antagonists including the "atypicals" have also been
implicated.

Symptoms of NMS begin within two weeks of initiation of the precipitating drug and mortality
rates range from 10-20%. The rigidity and hyperthermia of NMS may result in muscle necrosis,
reflected by elevated creatine kinase. Leukocytosis and electrolyte abnormalities are also
common. Immediate cessation of the causative agent is recommended.

Accidental Chemical Injuries of the Face/Eyes - In the case of any chemical contact with the
eye, the first priority is to immediately begin flushing the affected eye with copious amounts of
running water. This can best be achieved by holding the eyelid open under a running faucet for
at least 15 minutes before evaluation. Calling the emergency room, 911 , or the neighborhood
doctor would all be appropriate actions after initiating flushing of the eye. With exposure of the
eye to acid, there is a good chance of full recovery. With alkaline exposure, permanent corneal
damage is more likely to result. Regardless, flushing the eye with water is the appropriate initial
course of action for both cases.