Senior Repor 7.5

Case Presentation by Dr. Francesca Civitarese, DO

HPI:  Cinderella comes into the Pediatric Emergency Department with Prince Charming and their 3 kids, TreeStump (3), Sailfish (9), and Mike (6 months).

Cinderella isn’t sure, but she thinks that Treestump may have taken some of her medication while she was in the home spa and sauna with Prince Charming.

She accidently left her pill bottles on the table, and found 2 of the 6 pill bottles opened, with pills scattered all around the carpet when she was finished sweating to the 80s music in the sweat lodge.

She can’t remember some of the names of the pills, doesn’t remember which bottle was open, and didn’t bring the bottles.

Mom found Treestump after being in the sauna for approximately 1.5 hours.  Unknown actual time of ingestion.   She’s not sure if he took any of her medicines, but Sailfish (9yr old) told mom that Treestump said he wanted “some of moms candy” and so he opened the child proof caps for him.  He doesn’t know anything else other than that because he left the room.

When mom found Treestump around the bottles, she freaked out and brought him in after showering, fixing her hair, and changing her outfit a few times.  Upon arrival to the ED, she thinks it may be about 6 hours since she left the sweat lodge and found Treestump.  Initially he seemed to be fussier than usual to her, and irritable.  She said his crying sounded “high and squeaky, like a little girl”.  Right before she left, Treestump threw up, and in the car she says “he kept spitting up all over the place”. She was very confused, angry that her car now smells like vomit, and is near hysteria and can’t provide any other information.

They are triaged to resuscitation as a medical code for possible ingestion/overdose.

On initial examination of Treestump, he is looking all over the room and doesn’t seem to track physician or mom.  He is a little sleepy appearing.  He throws up in the ED and the emesis appears to be bloody but non-bilious.  He is not communicating anything to the staff, and mom says the only words he knows are “no”, “snack time”, and “daddy”.

Her medical problems:
Diabetes
Anemia
Hypertension
Fibromyalgia
Seasonal allergies

Her non-medical problems:
Drinks
Smokes weed
Married Prince Charming and named a child “TreeStump”

Background on Treestump:
3 year old male
Birth History:  born full term, no complications with pregnancy or delivery, 6#7oz, now weighs  27Kg
PMHx:  GERD as an infant, now resolved
PSHx: none
Allergies:  none
Meds:  none
Vaccines:  UTD
Exposures:  mom’s pills.
Family Hx:  as above.

PE:
VS:  BP 90/46   HR 145  RR30  T 99.4 temporal
GEN:  slightly sleepy appearing, but interactive.  Seems to be looking all around the room, but not at particular people or objects.  Appears to have a pale face and hands
HEENT:  NCAT PERRL, 3mm.  mucous membranes appear slightly dry.  Feels warm to the touch.  TMs clear.  Nares clear.  No pill residue on oropharynx
CARDS:  tachy, but regular.  No mgr
PULM: CTAB
GI:  mildly tender in the epigastric region, doesn’t seem to be guarding/rebound.
Rectal:  Heme positive
EXT:  wwp, skin dry.  No rashes.
MSK:  normoreflexic.  No clonus or tremor.  Normal tone and muscle bulk for age group.

INITIAL LABS:
Accu-check:  150
Cap Blood Gas:     pH 7.22, PCO2 29, PO2 78 HCO3 11

Lytes:  Na 131, Cl- 90, K 3.7, HCO3 12, BUN 22, Cr 1.1, Gluc 150

CBC:  WBC 15.1, Hgb 12, Hct 33.2, Plts 422

EKG:  was obtained and was normal for age

You send Serum Drug Screens, LFTs, a UDS, a UA, and coagulation studies, but these are not immediately available.

Questions:
1)     What is the correct interpretation of the ABG?
a.     Primary metabolic acidosis with complete respiratory alkalosis compensation
b.     primary metabolic acidosis with partial compensatory respiratory alkalosis
c.     primary metabolic acidosis with respiratory alkalosis and metabolic alkalosis
d.     primary metabolic acidosis with respiratory acidosis and metabolic alkalosis

2) What is an appropriate imaging or diagnostic study that most likely to help you in evaluating the patient?
a. abdominal xray
b. chest x ray
c. endoscopy
d. abdominal ultrasound
e. no imaging useful in this case

3) What is the appropriate medical therapy for Treestump?  Choose all that apply.
a. supportive therapy with IV fluids and antiemetics
b. deferoxamine
c. repeat accuchecks, D50 as needed
d. narcan
e. urine alkalinization
f. NAC
g. physostigmine
h. whole bowel irrigation.
i.activated charcoal

4)  After Treestump was admitted to the hospital, he developed (RLQ) abdominal pain, fever, and increasing diarrhea.  What established complication of this overdose did he develop?
a. nonspecific colitis
b. toxic megacolon
c.  C. difficile
d. gastroenteritis
e. Shigella infection
f. Yersinia infection

5)  How long should you observe Treestump in the emergency department before making the decision that he has survived his overdose and can leave, assuming all of his studies were negative and his symptoms resolve?
a. 4 hours
b. 8 hours
c. 12 hours
d. 16 hours
e. admit for observation

Bonus Question:  What is the ingestion that Treestump is least likely suffering from?
a.   sulfonylurea overdose
b.   iron overdose
c.   Benadryl overdose
d.  Norco overdose
e.  Tylenol overdose
f.   Salicylate toxicity
g.  Poly pharmacy

 

Answer & Discussion:
1) C
2) A
3) A, B & H
4) F
5) B

Question 1) ANSWER:  C

I:  the patient has an acidosis because the pH is low

II:  PCO2 is low (respiratory alkalosis) and the bicarbonate is low (metabolic acidosis) therefore the metabolic acidosis is the primary process

III: the anion gap is elevated at 29, therefore this is an anion gap acidosis

IV:  the patient has respiratory alkalosis compensation (partial)

V:  the delta gap is the measured serum anion gap – a normal anion gap (29-12) = 17

VI:  The delta-delta is the (delta gap + measured HCO3 (17+12)= 29.  Because the delta delta is above the normal HCO3, there is a concurrent metabolic alkalosis

Interpretation:
Primary elevated anion gap acidosis with partial respiratory compensation and concurrent metabolic alkalosis (likely 2/2 vomiting)

Bonus Question:  What is the ingestion that Treestump is least likely suffering from?
a.      sulfonylurea overdose
b.     iron overdose
c.     Benadryl overdose
d.     Norco overdose
e.     Tylenol overdose
f.     Salicylate toxicity
g.      Poly pharmacy

PEDIATRIC IRON TOXICITY
Iron Supplements generally contain Ferrous Sulfate (which contains about 20% elemental iron).  Most often, it is the children of post partum women (who have been placed on iron supplements after delivery) who can present with iron toxicity, although incidence, morbidity and mortality ARE declining overall.

Pediatric toxicity generally kicks in around 10-20mg/kg of elemental iron.  Serious toxicity/overdose starts at >60mg/kg.

It is important to calculate the estimated elemental iron load that the patient took.  There are various iron supplement formulations on the market now, all with different percentages of elemental iron:

  • Children’s multivitamin:  typically have 8-18mg of elemental iron per tab
  • Prenatal multivitamins:  325 mg of ferrous sulfate (contains 65mg of elemental iron per tablet)
  • Fe Sulfate:  20% elemental iron
  • Fe gluconate:  12% elemental iron
  • Fe fumarate:  33% elemental iron
  • Fe lactate:  19% elemental iron
  • Fe chloride:  28% elemental iron.

To Calculate the Ingested Iron:
Estimate the number of tablets.
Know the formulation of the iron supplement.
Know the milligrams on the iron supplement tablets and percent of elemental iron per tab.

1.  [total milligrams per tab * percentage elemental iron] = elemental iron in each tab in milligrams
then…
2.  take elemental iron in milligrams per tab, multiply by # of total tabs ingested.
3.  Divide this (the total elemental iron ingested in mg) by the patients weight in kg = ingestion in mg/kg

Iron has several effects on the body when taken in overdose. including local/systemic effects, GI corrosion and scarring, and derangements in metabolism. as well as effects on the heart, lungs, and liver.  Corrosive injury to the GI mucosa can result in vomiting/diarrhea/melena, and GI fluid loses, which ultimately can be so severe that they lead to hypovolemia.  Iron can cause focal erosive mucosal injury similar to that caused by a chemical burn. Endoscopically, this manifests as an erosion, an ulceration, or diffuse gastritis. Iron deposits a brown–black crystalline hemosiderin that erodes the mucosa. It is thought that iron erodes the mucosa through a direct corrosive effect that subsequently produces a local injury to the mucosa in a concentration-dependant manner.  You are more likely to have gastric effects from iron toxicity with pill or tablet iron supplements as opposed to liquid supplementation, with the theory being that the pill forms are more concentrated.

Although exact mechanisms are still uncertain, iron can also act as a direct cellular toxin that targets the liver and cardiovascular system with secondary CNS effects, metabolic acidosis from hyperlactemia, and free proton production from hydration of free ferric ions.  They can also present with coagulopathy from the liver toxicity effects.  Free iron is found to concentrate in the mitochondria. Oxidative phosphorylation uncoupling is a mechanism for cellular toxicity. There are other unknown mechanisms for cellular injury. Lactic acidosis results from tissue hypoperfusion/cellular hypoxia. Free iron may also cause direct damage to the heart leading to decreased myocardial contractility (negative inotropic effect on the myocardium). Coagulopathies may occur from effects of iron on clotting factors

Cardiac cell uptake and management of iron: mechanism
1

Ann N Y Acad Sci. Author manuscript; available in PMC 2010 June 28.
Published in final edited form as:
Ann N Y Acad Sci. 2005; 1054: 386–395.
doi: 10.1196/annals.1345.047

Iron toxicity is typically divided into phases, much like acetaminophen overdose, however presentations of iron overdose do not always fit this pattern, and should be used as a memory tool rather than a staging guideline.

PHASE I:  0-6 hours after ingestion
Mostly GI effects including hemorrhagic emesis, diarrhea, abd pain and cramping.  The theory is that elemental iron is corrosive to the gastric mucosa which can cause hematemesis.  Depending on the amount of GI losses and severity of the ingestion, during this phase the patient can start to develop metabolic acidosis, often secondary to tissue hypoperfusion from hypovolemia via third spacing

PHASE II:  4-12 hours post ingestion
“Latent” phase.”
Associated with a temporary symptomatic improvement, however laboratory studies may still show progressive worsening of the metabolic acidosis and may even show other evidence of end organ damage, including elevated transaminases – which can be used as a marker for liver damage from the ingestion

PHASE III:  12-24 hours post ingestion
During this phase, ferrous iron gets converted to ferric (Fe+++) iron, which liberates an unbuffered H+ ion. The ferric form of iron will then concentrate intracellularly in the mitochondria and disrupt oxidative phosphorylation, thus increasing the free radical production and lipid peroxidation processes.

This increases/worsens the metabolic acidosis that has been brewing in phases I and II, resulting in further cell death/tissue injury

GI:  increasing fluid losses, hypovolemia, acidosis worsens
CV:  HR decreases, decreased myocardial activity (etiology unclear), decreased CO (cardiac output), increased pulmonary vascular resistance
HEME:  coagulopathy

-free iron directly can inhibit formation of thrombin and thrombin’s effects on fibrinogen

-with severe toxicity and resultant hepatic damage, clotting factor production decreases due to hepatic toxicity/failure

Theory Behind AG Acidosis in Iron Toxicity

Several etiologies have been proposed, all of which may play a roll.
–     the conversion of free plasma iron to ferric hydroxide results in an accompanying increase in free H+ ion concentration in the body
–     free radical damage to the myocardial membranes prevents normal cell respiration/electron transport
–     hypovolemia results in hypoperfusion (i.e. increased lactic acidosis)
–     cardiogenic shock (uncertain etiology) results in tissue hypoperfusion = acidosis

PHASE IV:  2-3 days after ingestion
Iron is starting to be absorbed by the Kupffer cells and hepatocytes, and the storage capacity of ferritin is exceeded, resulting in oxidative damage in the liver.

This can result in periportal hepatic necrosis and will result in an increase in liver transaminases

PHASE V:  2-6 weeks after ingestion
Scarring of the GI tract
Can result in pyloric stenosis or hepatic cirrhosis

2) a – imaging modality in iron overdose
Chest X ray will not likely show the radiopaque iron tablets.  Endoscopy, although ultimately may be helpful in severe overdoses to assess overall mucosal damage/direct pill removal, will not be your initial imaging study of choice.  Abdominal ultrasound is unreliable for identification of iron ingestion due to bowel gas obstructing adequate view of gastric/intestinal contents.  Abdominal plain film x ray is helpful to identify radiopaque iron supplements, and can be used to estimate approximate ingestion severity.   It can also guide management as to whether or not to pursue whole bowel irrigation. Of note, many iron tablet formulations may actually NOT be radiopaque.  Ingestion severity should be gauged based on the patient’s overall clinical picture. If tablets are visualized in the stomach, obtaining an abdominal xray may be helpful for guidance of whole bowel irrigation.

Also remember that potassium chloride tablets can be radiopaque, as well as Chloral hydrate, calcium carbonate, iodinated compounds, acetazolamide, busulfan, and potassium preparations, and occasionally antihistamines, phenothiazines, and tricyclic antidepressants.
2

3) A, B, H

Treatment:
Current recommendations for acute symptomatic pediatric overdose 2/2 iron toxicity do not include inducing emesis (ipecac) or GI lavage currently (lavage makes already large iron tablets sticky and soggy, and does not aid in neutralization, symptom relief or removal of tablets).  Activated charcoal is not recommended currently for isolated iron toxicity/overdose because it doesn’t bind iron very well or absorb metals, but is recommended for possible polypharmacy ingestions. Always consider the patient’s airway when choosing to administer activated charcoal and gauge the patient’s current mental status.  Do not administer if risk of vomiting and aspiration (with potential loss of an airway) could be a strong possibility.

Whole bowel irrigation is recommended for pediatric population who are symptomatic in the moderate to severe overdose ranges, or in whom iron tablets can be identified on xray .

GoLYTELY ® (polyethylene glycol electrolyte solution) can be given orally or via NGT.  Irrigation should continue until there is a clear rectal effluent or until abdominal plain film no longer reveals any iron tablets present.

Dosing:  250-500ml/hour for toddlers/preschool aged children
2L/hour for adolescents

Deferoxamine (first-line chelating agent)
Indications for use:  patient with known or suspected iron toxicity who is in shock, has altered mental status, visible pills on abdominal xray, or persistant GI symptoms.  Also, for serum Fe+ level >500 micrograms per dL; or estimated ingestion >60mg/kg.

For Moderate Toxicity:  dosing within 6-12 hours after ingestion
For Severe Toxicity:  dosing up to 24 hours after ingestion

Can be given IM, or IV.  If giving medication IV, initial dosing is over a period of 6 hours with a goal rate of 15mg/kg/hour.  Rate should be started out lower, and gradually increased to goal

Side effects are rare, but can be pulm-toxic, including a rare side effect of ARDS and flash pulmonary edema .  This side effect has been most often seen in prolonged infusions.  Also, IV dosing can result in dose related hypotension, so use caution in administering this drug if the patient is already in shock

Deferoxamine mesylate (Desferal)
Freely soluble in H2O.  can absorb approximately 8mg iron per 100mg of drug. This may seem like we are only chelating a very small amount of the total elemental iron ingested, which may be the case in your patient.  However, we are using this to attempt to encourage clinical improvement, which can be achieved with even small amounts of chelation.

Deferasirox (Exjade)
PO tablet for chronic iron toxicity.  Decreases concentration of iron in patients who receive repetitive RBC transfusions.  Has a 2:1 binding affinity for elemental iron

4)  (F) Yersinia
Patients with iron overdose who are treated with deferoxamine are at risk for Yersinia infection.  DFO serves as a siderophore for Yersinia, that elemental iron as a growth factor, and it acts to solubilize iron and aids in intracellular entry for Yersina organism.  Suspect Yersinia infection in patients with iron toxicity that have been hospitalized and develop fever, diarrhea, increasing abdominal pain, or signs of sepsis.

5) b
it is generally accepted that if the patient is asymptomatic at 6-8 hours post ingestion, that severe iron toxicity is highly unlikely and that the patient can be safely discharged home.

You should expect to see clinical toxicity at 20mg/kg, and systemic toxicity at 60mg/kg.  Any ingestion that is over 250mg/kg is potentially lethal

TO REVIEW IRON TOXICITY CALCULATIONS/FORMULATIONS:
It is important to calculate the estimated elemental iron load that the patient took.  There are various iron supplement formulations on the market now, all with different percentages of elemental iron

  • Children’s multivitamin:  typically have 8-18mg of elemental iron per tab
  • Prenatal multivitamins:  325 mg of ferrous sulfate (contains 65mg of elemental iron per tablet)
  • Fe Sulfate:  20% elemental iron
  • Fe gluconate:  12% elemental iron
  • Fe fumarate:  33% elemental iron
  • Fe lactate:  19% elemental iron
  • Fe chloride:  28% elemental iron.

To Calculate the Ingested Iron:

Estimate the number of tablets.

Know the formulation of the iron supplement.

Know the milligrams on the iron supplement tablets and percent of elemental iron per tab.

1.  [total milligrams per tab * percentage elemental iron] = elemental iron in each tab in milligrams

then…

2.  take elemental iron in milligrams per tab, multiply by # of total tabs ingested.

3.  Divide this (the total elemental iron ingested in mg) by the patients weight in kg = ingestion in mg/kg

Serum Iron Levels:  estimated to peak at 2-6 hours post ingestion.   At greater than 8-12 hours after ingestion, the iron will have disseminated into the tissues, can result in a falsely low serum iron level.  After 6 hours, serum iron levels become unreliable.

  • Mild  Toxicity:  <300mcg/dL
  • Moderate Toxicity:  300-500mcg/dL
  • Severe Toxicity:  >500 mcg/dL

Additional Risk Stratification:

It has been suggested that WBC counts >15 and blood glucose levels >150 at presentation are perhaps correlated with more severe ingestions/toxicity potential, but this has been yet to be fully substantiated and is not necessarily a sensitive test

“Deferoxamine Challenge Test”
give a single dose of deferoxamine.  This medication will bind the available free iron and will excrete through the urine as a ferrioxamine complex, turning the urine a reddish color.  Urine red = lower threshold to chelate.  This is a inaccurate, not very scientific way to gauge whether or not the chelate the patient, and your decisions should always be based on the clinical picture of the patient as a whole, but sometimes additional information such as this can influence or help guide your direction of care.

Bonus Question:

(c) Diphenhydramine hydrochloride is an antihistamine commonly used for allergies and allergic reactions.  It is also present in other drug preparations such as Tylenol PM, Benadryl, Nytol, and Sominex.

Diphenhydramine is an H1- receptor antagonist that blocks the binding of histamine to the receptor sites and allows it to prevent allergic symptoms and inflammation.

Typical diphenhydramine dosing:  Adults can take 150-300 mg in divided doses (25-50 mg every 4 hours), whereas children can have 75 to 150 mg in a day in divided doses (12.5-25 mg three to four times a day).

Lethal levels of diphenhydramine in the blood include higher than 19 mg/L in adults, 7 mg/L in children and 1.5 mg/L in infants .

H1 receptor antagonist also competitively inhibits the muscarinic receptors resulting in the classic anti-cholinergic effects such as dry skin, dry mouth, tachycardia, urinary retention and delirium, and does not seem to fit Treestump’s clinical picture. Since diphenhydramine blocks neurotransmission through sodium block, it also can cause sedation and other CNS effects, that we are not really seeing on his exam.

Anticholinergic Symptoms

▪                Dry mucous membranes

▪                Flushed, dry, hot skin

▪                Low-grade fever

▪                Absence of sweating

▪                Dilated pupils

▪                Blurred vision

▪                Intestinal ileus

▪                Sinus tachycardia

▪                Urinary retention

▪   Anti-cholinergic delirium as evidenced by agitation, disorientation, confusion, poor short- term memory, meaningless motor movements and incoherent speech

References:
1.   The radiopacity of ingested medications.
Savitt DLHawkins HHRoberts JR. Ann Emerg Med. 1987 Mar;16(3):331-9.

2.  Iron chelation: an update.
Sheth S. Curr Opin Hematol. 2014 Feb 5. [Epub ahead of print]

3. Iron Toxicity
Clifford S Spanierman, MD; Chief Editor: Asim Tarabar, MD
http://emedicine.medscape.com/article/815213-overview

4.  Ng HW, Tse ML, Lau FL, Chu W. Endoscopic removal of iron bezoar following acute overdose. Clin Toxicol (Phila). Nov 2008;46(9):913-5. [Medline].

5.  Valentine K, Mastropietro C, Sarnaik AP. Infantile iron poisonings: challenges in diagnosis and management. Pediatr Crit Care Med. May 2009;10 (3):e31-33. [Medline].

6.  Bosse GM. Conservative management of patients with moderately elevated serum iron levels. J Toxicol Clin Toxicol. 1995;33(2):135-40. [Medline].

7.  Gumber MR, Kute VB, Shah PR, et al. Successful Treatment of Severe Iron Intoxication with Gastrointestinal Decontamination, Deferoxamine, and Hemodialysis. Ren Fail. May 1 2013;[Medline].

8. Lacouture PG, Wason S, Temple AR, Wallace DK, Lovejoy FH Jr. Emergency assessment of severity of iron overdose by clinical and laboratory methods. J Pediatr 1981 Jul;99(1):89-91.

9.  Goldfrank LR, Kulberg AG, Kirstein RM. Iron. In Goldfrank’s Toxicologic Emergencies, 3rd ed. Norwalk, Appleton-Century-Crofts, 1982.

10.  Management of acute iron poisoning.
Proudfoot ATSimpson DDyson EH. Med Toxicol. 1986 Mar-Apr;1(2):83-100.

11. Objectives and mechanism of iron chelation therapy.
Hershko C1, Link GKonijn AMCabantchik ZI. Ann N Y Acad Sci. 2005;1054:124-35.

12. Review of Oral Iron Chelators  (Deferiprone and Deferasirox)for the Treatment of Iron Overload in Pediatric Patients

D. Adam Algren, MD

http://www.who.int/selection_medicines/committees/expert/18/applications/OralIronChelators.pdf

3 Responses

  1. That was the longest case ever

  2. 1.
    Although… technically there is a concurrent respiratory acidosis (based on Winter’s formula the expected PaCO2 is 24-28 for an HCO3 of 12 and this PaCO2 is 29) and no evidence of a concurrent metabolic alkalosis (normal delta gap). But that choice isn’t listed.
    2. (Based on the possibility of seeing some radio-opaque iron tablets)
    3.
    4.
    5. I’m a little confused about the question. Is it a question about an asymptomatic patient with a negative laboratory workup, or is it a question about the patient in the this question whose remaining laboratory studies return normal? For the patient in this story (fairy tale?) he is already symptomatic with a significant metabolic acidosis and will require admission and probably ICU management (not listed as a choice). For an asymptomatic patient with a negatlive laboratory work up iron overdose (with some anticholinergics thrown in), with this time course, observation for 4 hours would be sufficient as any toxicologic effects would have shown up already (patient arrived at least 6 hours following ingestion). So.. … I guess
    Bonus:

  3. I have a few issues with the answers and discussion posted here:

    1. The primary disorder is a metabolic acidosis with partial compensatory alkalosis. There is also a concurrent respiratory acidosis (Winter’s formula). The Delta gap is what would be expected for a high anion gap metabolic acidosis. There is not a concurrent metabolic alkalosis.

    Here’s the formula:

    Delta Gap = Measured AG (29) – expected AG (12) – normal HCO3 (24) -measured HCO3 (12)

    That’s 5. Greater than 6 would be concurrent metabolic alkalosis and less than -6 would be concurrent non-gap metabolic acidosis. 5 is between 6 and -6.

    Bonus Question: The strange behaviors and general physical exam findings of tachycardia, dry skin, dry membranes, and even the “slightly sleepy” appearance ALL fit with a concurrent Benadryl ingestion.

    Thus for #3: One could consider administering physostigmine empirically, especially given that the EKG is noted to be “normal.” If the QRS duration was funky, then it wouldn’t be a good idea. Moreover, fulminant hepatic failure with resulting hypoglycemia, is a possibility in iron overdose, so at least until LFT’s come back, I think Q1 accucheks and D50 as needed is definitely indicated. Especially in the little people with their relatively sparse glycogen reserves.

    For #5: the answer does not take into account time since presentation. The patient is ALREADY 6 hours post ingestion. You gave us this in the story.

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