COW – Q 1.2

COW

*CASE OF THE WEEK*

HPI: 2-year-old boy with a history of eczema presents after a possible clonidine ingestion. The mother states that she put the child ton bed and upon checking on him later in the night, found him with an open pill bottle of 0.1 mg clonidine tablets. She apparently had left her purse reachable to the child. She is not sure if and how many pills the child ingested. Incident occurred at 11:00PM. The mother noticed the patient became lethargic and limp;  therefore, she brought him to the SG ED.

ROS: unable to obtain

PMH: Eczema

PSH: None

Meds: None

Social History: Lives at home with mother, shots UTD

Do you have a list of medications in the home?

Physical Exam

Blood pressure: 116/62, Pulse 123, Temperature 36.7, respiratory rate 20.

General:  Well nourished, Well developed, difficult to arouse with stimulation

Eye: Pupils are small, 2  mm, equal and reactive.

HENT:  Normocephalic, Atraumatic.

Respiratory:  Lungs CTA bilaterally.

Cardiovascular:  Tachycardic, S1 auscultated, S2 auscultated, No rub, No murmur, No gallop, Good pulses equal in all extremities, Normal peripheral perfusion, No edema.

Gastrointestinal:  Soft, Non-tender, Non-distended, Normal bowel sounds, No organomegaly.

Musculoskeletal:  Normal range of motion, No swelling, No deformity.

Integumentary:  Warm, Dry.

Neurologic:  Normal deep tendon reflexes, Not alert,  No clonus or other abnormal movements, Moving all four extremeties, Non focal exam.

LABS: 

ABG: 7.29/32/86/15

White count 6, hgb 10.9

APAP, salicylate undetectable

Electrolytes normal; What was the AG?

QUESTION 1:

QUESTION 2:

QUESTION 3:

BONUS QUESTION 4:

Presented by Dr. Andrew King. 

radER Case 13.2 (#14)

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Case

25 YOM presents to the ED complaining of sudden onset of right foot pain while playing football earlier today. He states that he was bearing all of his weight on his right foot at the time of the onset of pain. He states that his pain is significantly worsened with bearing weight and ambulation. He denies numbness and tingling. He denies any previous right lower extremity injuries. A right foot x-ray was obtained.

1. What abnormality should be identified in these radiographs?

2. What is the most common secondary/associated fracture involving the above abnormality?

3. Which statement is true of the proper treatment of the above injury?

Case 14 Answers

1. Correct Answer C. Lisfranc Fracture. Separation of the bases of the 1st and 2nd metatarsals should be evident in this film. It also appears as though there may be an avulsion fracture of the base of the 2nd metatarsal associated with the dislocation injury. No evidence of Jones or Pseudo-Jones fracture is noted in these views. No accessory bone is noted near the base of the 5th metatarsal to suggest Os peroneum. Os peroneum is very common seen in nearly 26% of foot x-rays and should not be mistaken for apophysis or avulsion fracture of the 5th metatarsal.

2. Correct Answer A. Base of 2nd Metatarsal Fracture is the most common fracture associated with a Lisfranc injury/dislocation.  Calcaneal fractures are not directly associated with Lisfranc dislocation fractures however should be suspected in MVC trauma patients that sustain Lisfranc injury. Cuboid fractures are seen as a result of Lisfranc dislocation however not as commonly as 2nd metatarsal fractures. Avulsion fractures of the 5th metatarsal are not commonly associated with Lisfranc dislocation.

3. Correct Answer B. ED Orthopedic consultation and evaluation. Lisfranc dislocation injuries all need to be evaluated immediately by an orthopedic surgeon. If unstable, surgery is the only corrective measure. The patient is to be NWB on the affected lower extremity. They should be placed in a short leg splint to stabilize/immobilize the foot and ankle.

Discussion:

Mechanism of Injury

  • Mechanism involves severe plantar flexion of the foot
  • May occur from sports-related injuries
  • Motor vehicle accidents
  • Falling from a height, down stairs or off a curb

Lisfranc ligament diagonally connects the 1st (medial) cuneiform with the base of the 2nd metatarsal. If it remains intact, either an avulsion of the lateral border of the 1st cuneiform or an avulsion of the base or medial border of the 2nd metatarsal occurs. If it tears, these fractures may not occur

Have a high index of suspicion as 20% of cases are undiagnosed due to other sustained trauma

Clinical findings

  • Pain at tarsal-metatarsal joints
  • Ecchymosis
  • Instability

Two basic types

A. Homolateral

  • All of the metatarsals are dislocated to the same side
  • More common than divergent
  • Usually involves the 2nd through 5th dislocated laterally
  • May involve all 5 metatarsals

B. Divergent

  • Usually more severe than homolateral
  • May be associated with a fracture of the 1st cuneiform
  • Usually involves medial displacement of the 1st metatarsal and lateral displacement of 2nd-5th metatarsals
  •  Occasionally may involve only medial displacement of only the 1st metatarsal

Fractures commonly associated with Lisfranc dislocations

  • Base of 2nd metatarsal (most common)
  • Cuboid
  • Fractures of shafts of metatarsals
  • Dislocations of the 1st (medial) and 2nd (middle) and cuneonavicular joints
  • Fractures of the tarsal navicular

Imaging

  • Conventional radiographs are usually sufficient to demonstrate the injury.

Normal alignment of the cuneiforms and the bases of the metatarsals

  • Lateral border of 1st metatarsal is aligned with lateral border of 1st (medial) cuneiform on AP view
  • Medial border of 2nd metatarsal is aligned with medial border of 2nd (intermediate or middle) cuneiform on AP view
  • Medial and lateral borders of the 3rd (lateral) cuneiform should align with medial and lateral borders of 3rd metatarsal on oblique view
  • Medial border of 4th metatarsal aligned with medial border of cuboid on oblique – Lateral margin of the 5th metatarsal may project lateral to cuboid by as many as 3mm on oblique
  • On lateral, a line drawn along long axis of talus should intersect long axis of 5th metatarsal

radER Case 13.1

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CXR PA s/p NGT

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Case 1 Questions

54 YOM presents to emergency department complaining of midsternal chest pain that he states has been coming and going for the past few years.  He states it has worsened over the past week becoming more constant.  He denies exertional component to his chest pain.  He denies any shortness of breath or difficulty breathing.  He does state that he intermittently feels nauseated but does not have any episodes of emesis.  He denies any fevers, chills, and productive cough.  He states that he has a history of hypertension, diabetes, and coronary artery disease with CABG x3.

The patient’s physical examination is unremarkable.

1. What significant abnormality is noted on the PA view of his patient’s chest film?
A. Acute Infiltrate
B. Increased Pulmonary Vascular Congestion
C. Esophageal dilatation
D. Westermark Sign

2. What is the most preferred initial screening/diagnostic test if the above condition is suspected?
A. Barium Swallow
B. CTA Thorax
C. D-Dimer
D. Echocardiogram

3. What is the preferred initial pharmacotherapy?
A. Heparin bolus with subsequent heparin ggt
B. Calcium Channel Blockers or Nitrates
C. Cetriaxone and doxycycline
D. Fondaparinux with warfarin overlap

Case 1 Answers

1. Correct Answer C. Esophageal dilatation with air-fluid level is the most notable abnormality on the PA view of his chest x-ray. This is often seen in an advanced achalasia as the lower esophageal sphincter as constricted and not allowed any liquid or solids to pass causing significant dilatation of the esophagus. No acute infiltrate is noted in the chest x-ray to suggest pneumonia.  No increased pulmonary vascular congestion is appreciated. Pulmonary embolism should be considered however no shortness of breath or history of DVT/PE exists.  No Westermark Sign is noted on his chest x-ray.

2.  Correct Answer A. Barium Swallow is the preferred initial screening test if achalasia is suspected.  Extensive esophageal dilatation is typically only noted 1 chest x-ray in advanced cases. A CTA thorax is the preferred modality for diagnosis of acute pulmonary embolus.  A d-dimer should only be used in the low risk patient’s suspected of having a pulmonary embolus with a Well’s score of less than 2. An echocardiogram is also a good screening test for both acute pulmonary embolism with right heart strain as well as for acute heart failure however it serves no role in the diagnosis of achalasia.

 3.  Correct Answer B. Calcium Channel Blockers or Nitrates are the preferred initial pharmacotherapy for smooth muscle relaxation in patients with achalasia.  Ceftriaxone and doxycycline are preferred for patient’s being admitted with acute community acquired pneumonia. Heparin bolus with subsequent drip is preferred in patients with acute pulmonary embolus that may undergo PCI. Fondaparinux with Coumadin overlap is preferred for stable patient’s with acute pulmonary embolus.

COW – answer 1.1

COW

*CASE OF THE WEEK*

You are working your first overnight shift at your new job right out of residency. Part of your contract is to cover a smaller satellite facility with limited resources that takes a steep dive at night.

The triage nurse rolls by your station with a young woman in a wheelchair. The nurse is moving with purpose, which makes you a little nervous. The patient is bent over and holding her abdomen. She holds an emesis basin on her lap.  It looks like there is a small amount of blood present.

She seems sleepy but arousable and is unable to give much of meaningful history.

The nurse gets her in bed and points to her gravid uterus. She grimaces and puts the patient on the monitor.

Her husband arrives. He says that she has been depressed and withdrawn recently, not sure why. She texted him an ambiguous farewell message a few hours ago. He hands you an empty bottle of prenatal vitamins.  He says that she just bought this a couple of days ago and is concerned that she took all of them.

ROS: Postive for abdominal pain and hematemesis, decreased mental status

PMHx:

Unknown

PSHx

Unknown

Meds:

? prenatal vitamins

SHx

Unknown

FHx

Unknown

Physical Examination:

P 110  BP 95/60  RR 12  T 36.5

Fetal heart tones are 135 bpm via bedside ultrasound

General: Young woman, lying in bed, fetal position, sleepy but arousable

HEENT: PERRL, EOMI, MMM

Neck: supple, no LAD

Heart: Tachycardic, clear S1 and S2. No murmurs. No extra heart sounds

Lungs: clear

Abdomen: Gravid uterus, about 30 cm from pubic bone

Extremities: Thready pulses. No c/c/e

Neuro: Sleepy. Follows commands. MAE x 4. Normal reflexes at knees and ankles. No rigidity.

LABORATORIES:

Na 138

K 3.4

Cl 108

HCO3 16

Glucose 168

WBC 16K

Hgb 9.8

Hct 29

Plt 233K

VBG 7.28/25/152

QUESTION #1: You are concerned about overdose. What component of the prenatal vitamin is most concerning?

A. Vitamin A
B. Folinic acid
C. Calcium
D. Iron
E. ascorbic acid

ANSWER: D. Because hypervitaminosis A can cause both toxicity in the mother and the fetus, prenatal vitamins are specifically formulated with reduced amounts of vitamin A.  Iron toxicity is the most concerning component of prenatal vitamins in overdose.

QUESTION #2: Which is not an indication for deferroxamine?

A. 2 hour iron level >300
B. 4 hour iron level >500
C. Metabolic acidosis
D. Lethargy/AMS

ANSWER: A. Deferroxamine should be considered in patient looks ill, has repetitive vomiting, lethargy, hypotension, metabolic acidosis, and an iron level >500 ug/dL. 4-6 Hour levels are preferred, however, iron poisoning is a clinical diagnosis. Clinicians should not rely on a single measurement and a normal iron level does NOT rule out toxicity.

QUESTION #3: What are potential adverse reactions of deferroxamine?

A. Discolored urine
B. Hypotension
C. ALI/ARDS
D. Ototoxicity
E. A and B
F. B and C
G. All of the above

ANSWER: F.  Deferoxamine chelates free iron throughout the body and minimizing disruption of oxidative phosphorylation and improves metabolic acidosis. Interestingly, deferoxamine does not chelate a large amount of iron; however, the small amount of free iron it does chelate leads to significant clinical improvement. Chelation of iron creates ferrioxamine and is eliminated by the kidneys. Ferrioxamine SHOULD cause a reddish color of the urine (so-called vin-rose urine). Deferoxamine should be started, titrated up, and continued while the patient remains ill.  Hypotension is rate-related. Cases of ALI and ARDS are usually described in those with prolonged therapy (>36-72 h of therapy).

History:

  • In the 1990s iron was the leading cause of poisoning deaths, at least reported to the Poison Center, among children < 6.
  • Ironically, this paralleled an effort to be more vigilant in prescribing prenatal iron
  • FDA required warning labels, blister packaging and limits on the # of pills dispensed
  • The requirement of industry to use blister packs have been subsequently overturned.

Pharmacology

  • Because iron is a transition metal, it can accept and donate electrons relatively easily and this feature is utilized in many biochemical process, most notably in the electron transport chain, myoglobin and hemoglobin.
  • The body cannot actively excrete iron, therefore, total body iron is regulated by absorption.
  • In iron-deficient states, iron uptake by the duodenum can increase to 95%.
  • In therapeutic dosing, certain functions are saturated and further uptake is limited, however, in overdose, oxidation and disruption of the GI mucosa allows iron to be absorbed by its concentration gradient.
  • Toxicity depends on the amount of ELEMENTAL IRON anticipated to be absorbed.
  • Calculating the amount of elemental iron in a given supplement depends on the molecular weight of the compound. See the table below for the percent elemental iron per formulation (Adapted from Goldfrank’s Chapter 40, table 40-1).
Formulation % elemental iron
Ferrous chloride 28
Ferrous fumarate 33
Ferrous gluconate 12
Ferrous lactate 19
Ferrous sulfate 20
  • Chewable vitamins tend to have lower concentration of elemental iron (10-18 mg) per tablet when compared to prenatal vitamins (65 mg) and, accordingly, fatalities have not been reported.

Pathophysiology:

  • Iron generates oxidative stress via the Fenton reaction and the Haber-Weiss cycle.

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  • These reactive oxygen species oxidize membrane lipids and damage GI epithelium.
  • Once absorbed, iron binds to circulating proteins, mainly transferrin
  • Once saturated, “free” iron is free to distribute to the various organs.

Free iron leads to metabolic acidosis by two main mechanisms:

  1. Disruption of ox-phos (buffer lost, usual H+ not incorportated into ATP)
  2. Ferric iron + 3H2O à Fe(OH)3 + 3 H+

Clinical Manifestations:

  • AS A MEMORY TOOL ONLY, you can think about the clinical manifestations in 5 stages:

Stage 1: GI distress from local tissue damage in the gut. Gi bleeding, bowel necrosis and hemodynamic instability.  Without vomiting in the first 6 hours, UNLIKELY TO GET SICK

Stage 2: “latent stage”.  GI symptoms have resolved  but develop AMS, metabolic acidosis,  and tachycardia.  THEY WILL APPEAR ILL.

Stage 3: “Shock stage” Coagulopathy, seizures, coma.

Stage 4: Hepatic failure

Stage 5: Chronic issues: GI scarring and stricture

Testing:

  • NOT ALL FORMULATION ARE RADIOPAQUE
  • Liquid and chewable formulations often will not show up on plain radiography
  • Follow electrolytes, ABG or VBG, lactate, coags, WBC (may suggest toxicity), APAP/Salicylate, EKG

DIAGNOSIS:

  • Diagnosis remains clinical
  • Peak iron levels are thought to occur between 2-6 hours post ingestion
  • Serum [Fe] 300-500 à GI and moderate systemic toxicity
  • Serum [Fe] 500-1000 à severe systemic toxicity and shock
  • Serum [Fe] >1000 à high likelihood of death
  • MUST FOLLOW SEQUENTIAL LEVELS, NOT A RULE OUT TEST
  • TIBC (total iron binding capacity) and ferritin are not useful, may lead to confusion, and not recommended

MANAGEMENT:

  • ABCs
  • IV fluids
  • Whole bowel irrigation
  • For patients with retained iron despite WBI may require EGD and/or surgical removal
  • Antidotal therapy

DEFEROXAMINE

  • Deferoxamine + Fe3+ à ferioxamine à Excreted by kidneys
  • Consider treatment if patient looks ill, has repetitive vomiting, lethargy, hypotension, metabolic acidosis, iron level >500 ug/dL
  • Intravenous administration should be increased to 15mg/kg/h.
  • Continue therapy until patient is clinically well.
  • Could consider dialyzing at the same time (animal studies exist)
  • ADVERSE EFFECTS:
  • Hypotension is rate-limiting factor
  • ALI and ARDS
  • PREGNANCY IS NOT A CONTRAINDICATION

Dispo:

  • AAPC guidelines are as follows
  • >40 mg/kg adult formulation or severe or persistent symptoms (alterations in level of consciousness, hematemesis, and bloody diarrhea, persistent vomiting), refer to ED (use pre-pregnancy weight for pregnant women)
  • All children’s chewable vitamins manage at home unless persist vomiting/diarrhea warrant IV fluids
  • All patients with carbonyl iron or polysaccharide-iron complex remain at home
  • Observe for six hours; if asymptomatic à home
  • Otherwise, admit

For pregnant patients: TREAT MOTHER as above.