Candy or Medication?

You’re working a busy shift in the peds ED among a seemingly endless cycle of various permutations of fevers, cough, abdominal pain, vomiting, diarrhea, when another kid pops up on the board: “vomiting, abdominal pain.” Fantastic. You go over to the kid and find a 4-year-old male with no significant past medical or birth history. Immunizations are UTD, and he is generally healthy. As per mom, he was in his usual state of health when he suddenly started to complain of generalized abdominal pain with multiple episodes of bloody vomiting and diarrhea for the last 3 hours. There have been no fevers, prior similar episodes, sick contacts, recent travel, recent antibiotics, or sketchy foods that the mom can recall. The kid mentions having eaten some candy earlier but won’t say from where he got it. The mom isn’t sure about that but mentions he may have gotten it from one of his older siblings, and in their family, the boys don’t snitch on each other. Physical exam demonstrates a boy in pain holding his abdomen who is afebrile, tachycardic, and somewhat toxic-appearing. It’s difficult to get a proper physical exam, but he seems to have generalized abdominal tenderness. Hmmm, this kid looks a little too sick than your run of the mill food-borne gastroenteritis. Maybe intussusception, inflammatory bowel disease, or foreign body??

What was it about that “candy”? The kid admits to getting the candy out of the mom’s purse. The mom gives a loud, “Huh? Say what, now??” And lo and behold, in the purse you find…

Image Source: http://www.vitaminsestore.com/17-causes-symptoms-and-treatment-of-iron-deficiency/

 

Iron Toxicity

Introduction and Brief Pathophysiology

Prior to 1990, iron toxicity used to be one of the major causes of toxicological deaths in children younger than 6 years. This was due to many factors including the medication’s resemblance to candy, presumed safety of iron-containing supplements, and simply not knowing that iron can be present in various multivitamin preparations in somewhat significant amounts (up to 100mg of elemental iron).1 Since then, public health efforts have increased awareness and education, and federal packaging regulations had mandated unit-dose packaging for meds containing >= 30mg elemental iron per dose. This has helped to significantly reduce the incidence of iron poisoning.2,3 Nevertheless, as EM docs, we have to be ready for anything that comes through those doors, so let’s take a further look into iron toxicity.

*Note: The federal regulations for unit-dose packaging has since been lifted by the FDA.4

Medications that resemble candy. Image Source: http://allparenting.com/my-family/articles/971239/watch-out-these-drugs-look-like-candy

 

How does iron toxicity present?

Described in textbooks as early as the 1950s,6 acute iron toxicity classically presents in 4-5 phases:

Phase Onset Presentation Remarks/Pathophysiology
1) Local/GI Toxicity 0.5-6h Nausea, vomiting, diarrhea, GI bleeding Redox reactions + free-radicals = damage to GI mucosa and increased passive absorption of Fe
2) Latent Period 6-24h Improving GI symptoms from phase I; however, progressive organ cellular toxicity and organ damage, metabolic acidosis This phase is not always present
3) Systemic Toxicity 12-24h Hemodynamic instability, shock, coagulopathy/DIC, metabolic acidosis 1) Negative inotropy

2) Decreased plasma volume

3) Inhibition of thrombin/coagulation cascade

4) Acidosis:

a) lactic acid due to shock

b) Inhibition of oxidative phosphorylation (protons normally used to form H2O are released)

c) Ferric hydroxide formation (Fe3++3H2O -> Fe(OH)3 + 3H+)

4) Hepatotoxicity <48h Hepatic failure Liver receives absorbed ions, iron from portal system, free-radical formation causes oxidative damage
5) Aftermath 3-6 weeks Intestinal obstruction Caused by strictures, fistulas, scars; gastric outlet obstruction most common

Table source: 1,8

 

Management:

ABCs, IV access, monitor. What was the question? Oh right, more specifics…

 

Diagnostic testing:

Calculate ingested dose of elemental iron (if possible)= [Amount of elemental iron in ingested formulation (refer to table below) x number of pills ingested]/weight in kg. As a GENERAL rule, the amount of ingested elemental iron can be risk stratified as follows:

– 20 mg/kg: mild symptoms start (nausea, vomiting, abdominal pain)1

– 40 mg/kg: cutoff of whether or not patient can be monitored at home or should be evaluated at a health care facility (as recommended by the American Association of Poison Control Centers). *If severe or persistent symptoms are present or the ingestion was intentional, this cutoff does not apply – the patient should be evaluated at a medical facility regardless of calculated ingested amount.6

– 60 mg/kg: severe toxicity1

Table Source: 6

 

Serum Iron Level is useful for diagnosis; should be measured at 4 hours after ingestion as peak levels occur at 4-6 hours after ingestion.1

<300 mcg/dL: less than upper range of body’s TIBC –> unlikely to be clinically significant1

>500 mcg/dL: moderate to severe toxicity8 – chelation therapy indicated7

>1000mcg/dL: severe toxicity, significant mortality8

 

CMP, Coags, VBG, Lactate may be helpful to assess for metabolic acidosis, coagulopathy, electrolyte imbalance, etc.

 

Also Not Absolutely Necessary But Can Be Helpful…

WBC, glucose may both be elevated in iron overdose, but these tests are neither sensitive nor specific.1 According to Goldfrank’s, one study found that WBC level of >15K or serum glucose of > 150 was found to be predictive of significant elevated iron concentration, but the results have not been replicated.14 It is important to remember normal WBC and glucose does not exclude toxicity.13

TIBC was once theorized to be helpful but has not proven to be reliable.1

 

Imaging:

KUB may be helpful for diagnosis and indicate need for whole bowel irrigation (WBI). See below. A negative KUB does NOT exclude iron ingestion or risk of toxicity.

 

Interventions:

1) In suspected iron overdose, you should involve your local Poison Control Center, (1-800-222-1222).

2) Supportive Care/Fluids – There may be fluid losses (vomiting, diarrhea) so replete with isotonic fluids, such as normal saline or lactated ringers.

3) GI decontamination – This is recommended for early presentation of massive ingestion or if pill fragments are seen on XR. However, it is not worthwhile if patient is already vomiting. Give polyethylene-glycol electrolyte solution (GoLytely) via NG tube at 500 ml/h (9mo-6y), 1000ml/h (6-12yr), 2000ml/h (>=13yr) until clear rectal effluent is achieved.9 Activated charcoal is not considered useful in these poisonings.

4) Deferoxamine (DFO) is a chelator of free iron.

Indications:1

– Serum iron > 500 ug/dL

– Significant clinical manifestations

– Significant metabolic acidosis

Dose:

IM: 50mg/kg q6hr, max 6g/24h

IV: max rate 15mg/kg/hr for 1 hour then lowered to 125 mg/h

– IV is more effective than IM

No clear guidelines of rate and duration of DFO. Expert consultation is recommended (i.e call your local Poison Control Center early at 800-222-1222).1

Major potential adverse effects

– Hypotension, renal failure, acute respiratory distress, sepsis due to Yersinia1,8

 

5) Other interventions that have helped in case studies in the past, but there are no clear indications or guidelines:

– Endoscopic removal of iron bezoar10

– Emergency gastrotomy has found iron embedded in gastric mucosa11

– Exchange transfusion/Plasmapheresis12

 

6) Interventions that are NOT proven to work and/or are not recommended:

Oral complexers, activated charcoal, cathartics, calcium EDTA, oral sodium bicarbonate, oral phosphates, sodium bisphosphonate, magnesium hydroxide, gastric lavage, hemodialysis/hemofiltration1

 

Disposition

Discharge if asymptomatic after 6 hours of ingestion, ingested elemental iron is < 40mg/kg, or if 4-6 hour serum iron level < 300 mcg/dL.

Otherwise, admit to regular floor or PICU depending on level of toxicity and severity of symptoms

 

Written By: Dr. Peter Song, PGY-2 Emergency Medicine at SUNY Downstate
Edited By: Dr. Caitlin Feeks, 2nd year PEM Fellow; Dr. Wiener, Associate Professor of Emergency Medicine and Medical Toxicology at SUNY Downstate; Dr. DeSouza, Associate Professor of Emergency Medicine at SUNY Downstate

 

Sources:

  1. Chang TP1, Rangan C. Iron poisoning: a literature-based review of epidemiology, diagnosis, and management. Pediatr Emerg Care. 2011 Oct; 27(10):978-85. doi: 10.1097/PEC.0b013e3182302604.
  2. Tenenbein M1. Unit-dose packaging of iron supplements and reduction of iron poisoning in young children. Arch Pediatr Adolesc Med. 2005 Jun; 159(6):557-60.
  3. Broderick M1, Dodd-Butera T, Wahl P. A program to prevent iron poisoning using public health nurses in a county health department. Public Health Nurs. 2002 May-Jun;19(3):179-83.
  4. Food and Drug Administration, HHS. Iron-containing supplements and drugs; label warning statements and unit-dose packaging requirements; removal of regulations for unit-dose packaging requirements for dietary supplements and drugs. Final rule; removal of regulatory provisions in response to court order. Fed Regist. 2003 Oct 17;68(201):59714-5.
  5. Wallerstein RO, Mettier SR. Iron in Clinical Medicine. University of California Press, 1958. pp 93-103
  6. Manoguerra AS1, Erdman AR, et al. Iron ingestion: an evidence-based consensus guideline for out-of-hospital management. Clin Toxicol (Phila). 2005;43(6):553-70.
  7. Leikin S, Vossough P, Mochir-Fatemi F. Chelation therapy in acute iron poisoning. J Pediatr. 1967;71:425Y430.
  8. Fine JS, Iron poisoning. Curr Probl Pediatr. 2000 Mar;30(3):71-90.
  9. Bouchard N. Current Guidelines For Gastrointestinal Decontamination In The Emergency Department. EM Practice Guidelines Update: 2010 Aug; 2(8): 8
  10. Ng HW, Tse ML, Lau FL, et al. Endoscopic removal of iron bezoar following acute overdose. Clin Toxicol. 2008;17:1Y3.
  11. Peterson CD, Fifield GC. Emergency gastrotomy for acute iron poisoning. Ann Emerg Med. 1980 May;9(5):262-4.
  12. Carlsson M, Cortes D, Jepsen S, et al. Severe iron intoxication treated with exchange transfusion. Arch Dis Child. 2008;93:321Y322.
  13. Goldfrank, LR et al. Goldfrank’s Toxicological Emergencies. Chapter 46: Iron. 10th McGraw-Hill Education; 2015.
  14. Lacouture PG, Wason S, Temple AR, et al; Emergency Assessment of severity in iron ovverdose by clinical and laboratory methods. J Pediatrics. 1981;99:89-91.

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Not So Bored When You’re the Obstetrician for the Night

You decide to take a break from the city and moonlight in a small rural hospital. You think you’ll be chilling for the night seeing urinary tract infections, or maybe you’ll finally see that snake bite you never thought you’d see. The night starts off slowly with a steady stream of patients complaining of abdominal pain and children with upper respiratory infections. Just when you were getting into the new groove of slow and steady for a change, you get a notification…

A 31 year-old gravid woman has sustained a gunshot wound to the head and neck. You are in a small rural hospital with no obstetrics service and no Neonatal ICU.

 

This image pops into your head and you think: if only it were this easy. Instead, you roll up your sleeves and snap back to reality, wondering how the night could suddenly have ended up like a mix between Grey’s Anatomy and Cloverfield.

The patient arrives.

Vital signs: BP 90/60, HR 140, RR 12, Pox 98% on room air

You start your evaluation with the primary trauma survey.

Airway: Intact, minimal swelling to the right side of the neck, no expanding hematoma

Breathing: Bilateral breath sounds with good chest rise

Circulation: Tachycardia, cool and clammy extremities, decreased capillary refill

Disability/Neurologic Assessment: Dilated left pupil, withdrawing to painful stimuli, unresponsive to verbal commands, GCS 6.

The patient is noted to have bleeding gunshot wounds to the left occipital region and right eye. Suddenly, her breathing becomes agonal. You intubate the patient as another member of the team activates the massive transfusion protocol. Two large-bore peripheral IV lines are placed and 1 L Lactated Ringer’s solution is started as O negative blood is being sent from blood bank. The patient becomes hypotensive (systolic BP 60s), bradycardic, and she exhibits decerebrate posturing.

Bedside sonogram reveals an IUP with a fetal heart rate.

Q1: When is the ideal time to perform perimortem caesarian section?
A perimortem caesarean delivery (C-section) should be performed within 5 minutes of maternal cardiac arrest to maximize survival chances for both the fetus and mother

Q2: When is perimortem C-section indicated?
Perimortem C-section is indicated only If gestational age is ≥ 24 weeks (in a setting of maternal cardiac arrest). If gestational age is < 24 weeks, continue maternal resuscitation

Q3: What factors are associated with an increased chance of fetal survival?
• Gestational age > 28 weeks • Fetal weight > 1kg • Short interval time between maternal cardiac arrest and delivery • Cause of maternal death not related to chronic hypoxia • Healthy fetal status prior to maternal death • Availability of neonatal intensive care facilities • Quality of maternal resuscitation

Q4: How do you perform a perimortem C-section?
   

Q5: How can you determine that gestational age is ≥ 24 weeks on physical exam?
By 20 weeks, the uterine fundus is palpable at the umbilicus; from 20-32 weeks the fundal height in cm approximates the gestational age

 

 

In your patient, the uterine fundus is palpable 6 cm above the level of the umbilicus, corresponding to an estimated gestational age of 26 weeks. Your patient further deteriorates into cardiac arrest. ACLS is started, and O neg RBC are given with rapid infusion, but after three minutes, there is no return of spontaneous circulation. CPR is continued on the mother as your attending makes the call to perform a c-section. On the field are your scalpel, mayo scissors, clamps, and everything else in the emergency c-section kit you’d never thought you’d open. Your attending looks over and hands you the scalpel. She says, “You’re a Kings County resident, you can handle this, right?” You make a vertical incision through the abdominal wall. The rest is history. The mother does not make it, but the baby survives.

For more reading check out the link below on neonatal resuscitation:

Neonatal Resuscitation

An Ob/Gyn attending shows up an hour later and offers you a spot in a nearby Ob/Gyn residency program as a PGY-2, but you politely decline.

References:

  1. Lanoix et al. Perimortem Cesarian Section: Case Reports and Recommendations. Acad. Emerg. Med. 1995; 2:1063-1067.

  2. http://adelaideemergencyphysicians.com/2016/03/thinking-about-perimortem-caesarean-section/

  3. https://www.acep.org/clinical—practice-management/time-is-critical-for-success-in-perimortem-c-section/

  4. AJOG 2005;192:1916-21. http://www.ncbi.nlm.nih.gov/pubmed/15970850

  5. Tintinalli’s Emergency Medicine

  6. Roberts & Hedges Clinical Procedures in Emergency Medicine 6ed

 

 

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