UNIVERSIDAD DE ZAMBOANGA

PAGADIAN BRANCH, INC.

Zone 4, Airport Rd., Brgy. TIguma, Pagadian City

Telephone No. 215-8148

Name: Weliam Jhay P. Coyme

Clinical Toxicology Laboratory

Activity 4
Case Study
(No. 6-11)

Case Study #6: Digitalis Poisoning

History:
A 3-year-old girl is rushed into the Emergency Department carried by her frantic mother. The
mother states that the child just consumed “a bottle of heart pills.” The mother and the patient
were apparently visiting the patient’s grandmother this afternoon, when the mother discovered
her daughter playing in the bedroom with an open bottle of pills. The bottle was labeled
“digoxin 0.25 mg tablets,” and there were 10 left. The Grandmother estimated that there were
probably 40 pills in the bottle this morning when she took her usual dose. Since the child had
been playing alone for some time, the ingestion could have occurred anytime within the past 90
minutes.
Physical Examination:
T: 99.4°F HR: 40 bpm RR: 30 breaths per minute BP: 98/52 mm Hg
Weight: 33 pounds (15 kg)
General: Age appropriate, lethargic female, whimpering and whining in the bed. Responds
irritably to any
stimuli. There are no signs of trauma.
Pulmonary: Clear to auscultation.
CV: Bradycardic, regular rhythm.
Initial EKG shows sinus bradycardia with first degree AV block.
Bedside glucose: 84
QUESTIONS
1. What tests would be appropriate in this case?
After securing the patients ABC’s and initiating intravenous access, continuous cardiac
monitoring and pulse oximetry, an ECG would be the initial test of choice. Also checking the
serum digoxin level. Note that serum digoxin levels are not reliable until approximately 6 hours
after last ingestion and that prior to this time they will appear elevated secondary to incomplete
drug distribution.
2. What therapy would you recommend and how much would you give?
The treatment of choice is digoxin-specific antibody (Fab) fragments. Derived from
immunized sheep, digoxin-specific antibody fragments are the Fab portion of IgG antibodies
that bind free digoxin in the serum so it can be renally excreted. Its administration in acute
ingestions with steady state levels greater than 10 ng/mL, chronic ingestions with steady state
levels greater than 4 ng/mL, and acute ingestions of greater than 10 mg in adults and 4 mg in
children.

3. What therapy for hyperkalemia should be avoided in this case?

Based on two case reports by Bower et al in the early 1900’s, the use of calcium in
digoxin-poisoned patients with hyperkalemia has been considered dangerous due to a
theoretical propensity to precipitate fatal ventricular fibrillation, or stone heart syndrome, by
increasing intracellular calcium. Most sources recommend avoidance of calcium administration
in these hyperkalemic, digoxin poisoned patients. Additionally, potassium lowering treatments
should be used judiciously in these patients because hypokalemia can precipitate digoxin-
induced arrhythmias.
Case Study #7: Beta-Blocker Poisoning
History: A 6-year-old white male presents to the emergency department with his parents after
accidently ingesting one nadolol tablet. One hour following the ingestion, the child became
dizzy and vomited. Because the child appeared to be very sleepy, the parents brought him in for
evaluation.
PMH: None.
Physical Examination:
T: 98.6°F HR: 100 bpm RR: 22 breaths per minute BP: 100/60mm Hg
General: Sleepy, but easily aroused.
HEENT: Normocephalic, pupils equal and reactive to light.
Pulmonary: Clear to auscultation.
CV: Regular rate and rhythm.
Neurologic: Unremarkable.
QUESTIONS
1. What are the most common clinical effects associated with β-blocker overdoses?
The most common signs associated with beta-blocker overdoses are bradycardia and
hypotension. More severe cases can result in AV block, cardiogenic shock and asystole. Rare
effects include hypoglycemia because beta blockers can inhibit glycogenolysis. Also
bronchospasm because it blocks the AV that causes bronchospasm.
2. What management should be instituted if the patient’s heart rate is 40 bpm?
Immediate therapy includes stabilizing the ABC’s. Intravenous access, supplemental
oxygen, cardiac monitoring and continuous pulse oximetry should be instituted immediately.
Symptomatic hypoglycemia should be treated in the usual fashion and benzodiazepines should
be used to halt seizures. Initial treatment measures include bolus administration of crystalloid
fluid, atropine and glucagon. Glucagon is to promote or stimulate the glycogenolysis to combat
the hypoglycemia if he has it. Also epinephrine to increase the blood pressure to combat low
bp.

3. What is the mechanism by which β-blockers cause toxicity?

 The primary mechanism of β-blocker poisoning is by excessive β-adrenergic blockade on
cardiac myocytes, which leads to decreased intracellular CAMP. This results in negative
inotropic, chronotropic and dromotropic effects on the heart and peripheral vasoconstriction.
Case Study #8: Theophylline
History:
A 12-year-old female was brought to the Emergency Department by her family with the
complaint that their daughter had exhibited gross twitching of her upper and lower extremities,
her eyes rolling back in her head with drooling from her mouth and urinary incontinence. This
activity was noted on two occasions within the last half hour and each episode lasted for
approximately 2-3 minutes. The mother stated that the patient has never exhibited any similar
activity. The mother states thatthe patient recently was very upset after having failed a major
exam in mathematics. The father reports he found an empty pill bottle at home which had
contained approximately forty 100 mg tablets of theophylline.
PMH: Asthma.
Medications: Theophylline.
Physical Examination:
T: 99.3°F HR: 130 bpm RR: 30 breaths per minute BP: 140/98mm Hg
General: Lethargic white female without any seizure activity.
HEENT: Pupils 4mm, equal and reactive to light bilaterally. No nystagmus.
Pulmonary: Clear to auscultation.
CV: Tachycardic, regular rhythm.
Abdomen: Unremarkable.
Neurologic: Diffuse hyperreflexia (3+) with down goingBabinski bilaterally.
QUESTIONS
1. What are your immediate concerns with this patient? What lab work, x-rays or ancillary
measures would you request?
The immediate concern should be finding the etiology for the patient’s seizures and
controlling/preventing any recurrent seizures. Immediate laboratory tests should include
electrolytes, glucose, BUN, creatinine, LFTs, U/A, CBC with differential, stat theophylline level
and toxicology screen including acetaminophen level. Radiographic examination should include
portable CXR, KUB and a head CT.
2. Based upon the above history, physical and laboratory results, what further treatment(s)
would you initiate for this patient?
Initial treatment includes airway, breathing, and circulation. Activated charcoal should
be administered after the airway is managed in this patient. Multiple doses should be
considered and whole bowel irrigation should be considered if a sustained release preparation
was ingested. Seizures should be controlled with benzodiazepines or phenobarbital; however,
theophylline seizures can be resistant to treatment. Theophylline can be removed with
hemodialysis or charcoal hemoperfusion; these should be considered in acute intoxication with
levels greater than 80mg/L, chronic intoxication with levels greater than 40mg/L, or persistent
symptoms such as seizures, hypotension, or dysrhythmias. Multiple doses of activated charcoal
can be used but is most effective with levels less than 100mg/L in acute intoxications.
Case Study #9: Cyclic Antidepressant Poisoning
History:
A 34-year-old female presents to your Emergency Department via EMS. Her husband states he
found her sleeping when he returned home from a business trip and became concerned when
he was unable to awaken her. She has been treated for depression recently. There was an empty
bottle of amitriptyline (prescription filled two weeks ago) andan empty bottle of diazepam
(prescription filled today) near the bedside.
Physical Examination:
T: 100.1°F HR: 118 bpm RR: 8 breaths per minute BP: 90/60 mm Hg
General: There are no signs of trauma.
HEENT: Mucous membranes are dry. There is no gag reflex. Pupils are dilated bilaterally and
sluggishly
reactive.
Pulmonary: Clear to auscultation.
CV: An irregular, tachycardic heart rhythm.
Abdomen: Soft with diminished bowel sounds.
Skin: Warm and dry.
Neurologic: Decreased level of consciousness. Slurred speech, responds to pain. Initial EKG
shows sinus
tachycardia with prolonged QT interval and QRS duration of 0.16 msec.
QUESTIONS
1. What are characteristic findings of TCA ingestion?
Patients with cyclic antidepressant (CA) toxicity present with signs and symptoms of
anticholinergic toxidrome and usually have decreased level of consciousness. They also may
develop seizures and, due to its sodium channel blocker properties, may develop cardiovascular
toxicity.
2. What drugs are contraindicated in this case?
 Both physostigmine and flumazenil are contraindicated in the treatment of TCA toxicity.
Also contraindicated are type IA, IC, II and IV antidysrhythmics.

3. What treatment would you institute in this case?

Initial treatment should focus on assessment of airway and breathing. Endotracheal
intubation should be performed in patients with signs of respiratory depression. The treatment
of choice for hypotension, unresponsive to fluids is also bicarbonate.
Case Study #10: Benzodiazepine Poisoning
History:
A 16-year-old female presents to the Emergency Department via private vehicle barely
responsive to painful stimuli. An hour ago, she informed her sister that she had “taken all of
Mom's diazepam,” which her sister estimates to have been about 20 tablets (5 mg), and washed
them down with “a bottle of vodka.” The reason for the delay in arrival was that she refused to
be transported, so her sister waited until she “passed out” to put her into the car and drive her
to the Emergency Department.
Physical Examination:
T: 98.8°F HR: 78 bpm RR: 6 breaths per minute BP: 126/86 mm Hg
General: Groans in response to painful stimuli. There are no signs of trauma.
HEENT: Pupils are mid-position, equal and sluggishly reactive. She has a
diminished gag reflex.
Pulmonary: Clear to auscultation.
CV: Regular rate and rhythm.
Neurologic: Neurological exam is without focal deficit.
QUESTIONS
1. What is most likely responsible for this patient’s respiratory depression?
The patient’s respiratory depression is most likely the result of the ethanol co- ingestant.
Oral benzodiazepine poisoning alone rarely causes respiratory compromise, and these patients
instead often present with CNS depression and normal vital signs.
2. Would you administer flumazenil to this patient?
The use of flumazenil in the treatment of acute overdose is debatable. The potential to
prevent invasive procedures like lumbar puncture is cited as a benefit of this antidote. The
patient's age and home access to diazepam may raise concerns about the possibility of a chronic
component of use in this adolescent, so this should be carefully considered before flumazenil
administration.
3. What is the dose of flumazenil?
 The initial dose of flumazenil is 0.2 mg given intravenously. When using flumazenil in
attempt to reverse the effects of acute overdose, patients who do not respond to an initial dose
should be given subsequent doses of 0.3 mg, followed by 0.5 mg. This can be repeated until a
total dose of 1 mg is reached.
Case Study #11: Phenytoin Poisoning
History:
A 19-month-old male presents to your emergency department with his parents after ingesting
35 mL of phenytoin suspension. Parents relate that he appears to be “wobbly” and “sleepy”. He
has had no vomiting and no seizure activity.
PMH: Brain aneurysm, seizure disorder, feeding disorder.
Physical Examination:
T: 100.4°F HR: 132 bpm RR: 30 breaths per minute BP: 110/70mm Hg
General: He appears very sleepy but is arousable and has an intact gag reflex.
HEENT: Examination reveals horizontal and vertical nystagmus. Mouth examination reveals
gingival
hyperplasia.
Pulmonary: Clear to auscultation.
CV: Regular rate and rhythm without murmur, capillary refill normal.
Neurologic: GCS = 15, cranial nerves II-XII intact. Truncal ataxia is present. Hyperreflexia present,
all
DTR’s.
QUESTIONS
1. What are the usual signs of acute phenytoin toxicity?
Mild to moderate intoxication causes horizontal nystagmus, ataxia, ophthalmoplegia, dysarthria,
hyperreflexia, hyperglycemia, irritability and altered mental status. Severe intoxication causes stupor,
coma and respiratory arrest. While phenytoin toxicity can produce paradoxical seizures, this finding
should prompt a search for other causes as this is a rare finding.

2. What initial therapy should be instituted?

Initial management is focused on stabilizing ABC’s. Patients with ataxia should have precautions
taken to prevent injury from fall. If seizures occur, treat in the usual way and search for other causes. In
the appropriate situation, activated charcoal may be administered. If the level is very high and the
patient has significant symptoms, multi-dose activated charcoal can be given to enhance phenytoin
elimination but is not necessary and may increase aspiration risk in symptomatic patients.

3. What are the signs and symptoms of chronic phenytoin toxicity?

Patients on long term phenytoin therapy can develop gingival hyperplasia, which is the most
common adverse effect in adults and children. Chronic phenytoin [11] © Ohio Chapter, American College
of Emergency Physicians [Link] toxicity may result in phenytoin encephalopathy. Other
adverse effects include hyperglycemia secondary to impaired insulin secretion, hypothyroidism,
osteomalacia, aplastic anemia, malignant lymphoma, hemorrhagic disease of the newborn (responsive
to vitamin K), and megaloblastic anemia secondary to decreased folate absorption and altered folate
metabolism (responsive to folic acid).