VLS 1.5


Image - Dacryoadenitis and dacryocystitis

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:
Seasonal allergies

Her non-medical problems:
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.

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
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.

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.

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

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

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
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

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.

3) A, B, H

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

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


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

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

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


VLS 1.4


image - Pterygium

Senior Report 7.4

Case Presentation by Dr. Erin Murphy

CC: “I’m having back pain.”

HPI: 63yo male presents to ED c/o abdominal pain & left flank pain x 2-3 days as well as cough, shortness of breath and intermittent sweating/chills. He describes the abdominal pain as diffuse, constant, achy, 10/10 in severity today and radiating to his low back. His left flank pain is sharp, constant & severe. He has nausea & vomiting today. The patient saw his PCP recently, was thought to have possible kidney stone & was prescribed Norco and Flomax. He denies urinary symptoms or diarrhea. Today, he is nauseated and has vomited several times. Denies hematemesis.

Constitutional: +subjective chills
ENT: No sore throat
Respiratory: +difficulty breathing
Cardiovascular: No chest pain
GI: +abdominal pain, no bloody stools
GU: No hematuria
Musculoskeletal: No arthralgias
Skin: No rash
Neuro: No weakness

PMH: anxiety/panic attacks, HTN
PSH: left hand surgery
Meds: clonazepam, acetaminophen-hydrocodone, paroxetine, tamsulosin
Allergies: NKDA
Social: smokes 1ppd cigarettes, denies alcohol

Physical Exam:
Vitals: BP 169/124 Pulse 80 RR 16 Temp 36.9 oral Pulse ox 90% room air
Constitutional: obese male, moderate distress, slightly diaphoretic
HEENT: no conjunctival pallor, sclera anicteric, oropharynx is dry
Respiratory: mild tachypnea, bibasilar crackles, no wheezes
Cardiovascular: regular rate & rhythm, S1, S2, no murmurs or gallops
Abdomen: obese, soft, no abdominal tenderness
Back: no CVA tenderness
Musculoskeletal: no pedal edema
Skin: no rash
Neurologic: awake, alert & oriented x3, no focal deficits

Emergency department course:
After the patient was evaluated by the physician, he was standing up to urinate when he suddenly collapsed onto the stretcher, became unresponsive & was found to be pulseless with agonal respirations. Cardiac monitor showed PEA, patient was intubated and resuscitated per ACLS protocol and had spontaneous ROSC but remained hypotensive despite aggressive fluids & pressors. CT-abdomen/pelvis with IV contrast was obtained.

murph 1

1. What is the above diagnosis?
a. ruptured perinephric hematoma
b. intra-abdominal abscess
c. ruptured AAA
d. spontaneous adrenal hemorrhage

2. Which of the following is NOT a risk factor for the above condition?
a. family history
b. diabetes
c. smoking
d. male gender

3. What is the next step in managing this patient?
a. Go to OR
b. CTA of abdomen and pelvis
c. bedside ultrasound of abdomen
d. angiograph

Answers & Discussion:
1) c
2) b
3) a

A true aortic aneurysm is a localized dilatation of the aorta caused by weakening of its wall; it involves all three layers (intima, media, and adventitia) of the arterial wall. This should not be confused with aortic dissections and pseudoaneurysms.

Rosen’s 7th Ed. Figure 84-1.

Aneurysms can develop in any segment of the aorta, but most involve the aorta below the renal arteries. The diameter of the normal adult infrarenal aorta is approximately 2 cm, and a diameter of 3 cm or more defines an AAA.

An AAA is a disease of aging. The average age at the time of diagnosis is 65-70 and men are affected much more often than women. The patient often has atherosclerotic occlusive disease of other vessels. Smoking is strongly associated with AAA. A family history of an AAA is a very strong risk factor; those with an affected first-degree relative have a 10- to 20-fold increased risk of developing an AAA. Female sex, African American race, and presence of diabetes mellitus are negatively associated with AAA.

AAAs progressively enlarge, ultimately resulting in rupture of the aneurysm and fatal hemorrhage. The most important factor determining the risk of rupture is the size of the aneurysm. The rupture risk increases dramatically with increased aneurysm size, and most ruptured AAAs have diameters greater than 5 cm. Rupture of an AAA usually occurs into the retroperitoneum, where hemorrhage may be temporarily limited by clotting and tamponade at the rupture site. Of patients with ruptures, 10 to 30% have free intraperitoneal rupture, which is often rapidly fatal. Complications can also arise from intact AAAs. The walls of AAAs are often lined with clot and atheromatous material, which can embolize and occlude distal vessels.Aortic thrombosis may occur rarely. Patients can also have complications caused by impingement on adjacent structures, like vertebral body erosion.

Patients with unruptured AAA may have symptoms, such as pain in the abdomen, back, or flank; an awareness of an abdominal mass or fullness; or a sensation of abdominal pulsations. The pain associated with stable, intact aneurysms has a gradual onset and a vague, dull quality. It is usually constant but may be described as throbbing or colicky. Acute or severe pain is an ominous symptom that suggests imminent or actual aortic rupture.

The most consistent physical finding is a pulsatile, expansile abdominal mass. There is virtually no risk of causing aneurysm rupture by abdominal palpation.However, an AAA may be difficult to palpate if the patient is obese. Most intact AAAs are nontender; tenderness suggests aneurysm expansion or rupture. The classic triad of a ruptured AAA is pain, hypotension, and a pulsatile abdominal mass,many patients have only one or two components of this triad, and an occasional patient has none of the classic features. Most patients with a ruptured AAA experience pain in the abdomen, back, or flank. Pain is usually acute, severe and constant. An AAA can rupture into the gastrointestinal tract (aortoenteric fistula) or inferior vena cava (aortocaval fistula) and should be suspected in patients with suspected AAA who are presenting with GI bleed or signs & symptoms of a large AV fistula.

Because of its low sensitivity compared with CT and ultrasound, plain abdominal radiography should not be used to investigate possible AAA. AAA’s may be incidentally seen on CXR as curvilinear calcification of the aortic wall or a paravertebral soft tissue mass.

Rosen’s 7th Ed. Figure 84-2

Ultrasonography is extremely sensitive in detecting AAAs, provided that a technically adequate study can be obtained (sometimes the aorta is not well visualized because of obesity or excess bowel gas). Ultrasonography has distinct advantages in the emergency evaluation of a patient with a possible ruptured AAA.It can be performed very rapidly at the patient’s bedside, obviating the need to take a potentially unstable patient to the radiology suite. If an aorta has a normal diameter visualized throughout its abdominal course, the patient does not have an AAA. However, ultrasonography cannot be relied on to determine whether an AAA has ruptured. The sensitivity of emergency ultrasonography in detecting extraluminal blood is very low. If ultrasonography reveals an AAA in an unstable patient, aneurysm rupture is presumed, and the patient requires immediate aneurysm repair.

Rosen’s 7th Ed. Figure 84-3. Cross-sectional ultrasound of a 6-cm abdominal aortic aneurysm. Note mural thrombus and eccentrically shaped patent lumen.

muprh 2j
Probe placement.

As with ultrasonography, abdominal CT is virtually 100% accurate in determining the presence or absence of an AAA and provides accurate measurements of the aortic diameter.CT is less subject to technical problems and interpretation errors than ultrasonography and is much more sensitive in detecting extraluminal blood. IV contrast is desirable, but not essential, in emergency situations. Obtaining CT is appropriate only in hemodynamically stable patients.

The patient with a ruptured AAA is unstable until the aorta is cross-clamped in the operating room or stabilized with endovascular techniques. No patient with a known or suspected aortic rupture should be considered “stable,” regardless of the initial vital signs or initial hemoglobin level.

When the patient arrives at the ED, large-bore IV access should be established and blood sent for crossmatching. Because patients with ruptured AAAs often have large transfusion requirements, at least 6 U of blood should be made available initially, with notification to the blood bank of the potential need for significantly more.The surgical and anesthesia team should be notified immediately. The hemodynamically unstable patient in whom a ruptured AAA has been diagnosed or is strongly suspected should be taken to the operating room as soon as possible. Attempts to resuscitate hypotensive patients fully in the ED and normalize the vital signs should be avoided. If transfer is required, it should be initiated as soon as the diagnosis is known or strongly suspected. Attempts to stabilize the patient in the ED are often fruitless and waste valuable time.

The appropriate degree of preoperative volume resuscitation is controversial. No prospective studies have compared different preoperative fluid regimens in hypotensive patients with ruptured AAAs, and the optimal resuscitation strategy has not been determined. The goal is to prevent irreversible end-organ damage without over-resuscitating to the point that clots may become dislodged and worsen bleeding. Although blood pressure necessary for vital organ perfusion varies among patients, a systolic blood pressure of 80-100 mm Hg is a reasonable target.


Key points:

  • An infrarenal diameter >3cm defines an AAA
  • Risk factors include age >65, male sex, smoking & family history
  • Risk of rupture greatest with aneurysms >5 cm
  • Acute or severe pain is an ominous symptom
  • Classic triad of a ruptured AAA = pain, hypotension & pulsatile mass
  • Maintain high clinical suspicion, especially in elderly
  • Bedside ultrasound is very effective at detection of AAA
  • Patients should be taken to OR as soon as possible

VLS 1.3


Image - Orbital cellulitis

Senior Report 7.3

Case Presentation by Dr. Jamie Kenney-Kalbuneh

47 year old male presented to the emergency department with the chief complaint of weakness.  Over the past two days he had progressively worsening weakness of his upper and lower extremities.   Two days prior his legs felt weak and he was unsteady when walking around the house.  It became gradually worse over the next 24 hours to the point he was unable to get out of bed.  The evening prior to arrival in the ED he noticed his arms became weak and he was unable to dress himself the next morning.  He also noticed that it was becoming hard for him to hold his head up and he began experiencing a tingling sensation in his hands and feet.  Patient had missed his last dialysis session due to having a recently clotted A-V Fistula.  He last received dialysis four days prior with no complications.

The patient denied shortness of breath, chest pain, cough, weight loss, nausea or vomiting.  No symptoms of fecal or urinary incontinence.  Denied any history of fever or chills, denied any sick contacts or recent travel.  No history of trauma.  Denied any new medication or changes to the dosing of his medication.

PMHx: HTN, SLE and ESRD secondary to lupus nephritis

SOCIAL:  Tobacco use, ½ ppd x 20years, negative for alcohol or drug use.

MEDICATIONS: Metroprolol, Amlodipine, Phoslo, Vitamin D, acetaminophen with hydrocodone

Constitutional:  Well developed middle age male in no acute distress.  He was resting comfortably on the stretcher and speaking in complete sentences.

Vital signs: BP 221/111 HR 71 RR 18 Temp 35.1 and Pulse ox 98% on room air.

Skin: Warm and dry, normal capillary refill.  Radial and dorsalis pedis pulses were 2+ and equal bilaterally.

HEENT: Normal cephalic, no signs of trauma.  Pupils 3mm and equal, EOMI.  No visual field deficits.  Moist mucus membranes, no intraoral lesions or thrush

Neck: Trachea midline, no JVD.  When patient was asked to turn his head toward one shoulder or lift his head off the bed he was unable.  When his head was passively lifted off the stretcher it would fall back down.  No neck pain, neck was supple.

Lungs: CTABL with normal respiratory effort

CV: S1/S2 regular rate and rhythm

Abdomen: Soft, non-tender to palpation, normal bowel sounds.

Rectal: Guaiac negative stool, normal rectal tone and a normal sized, non-tender prostate.

Musculoskeletal: No edema, no atrophy

Neurological: Patient was awake, alert and oriented. No facial asymmetry or dysarthria.  No nystagmus or clonus.  Follows commands appropriately.  No tounge deviation. Strength in bilateral lower extremities was 0/5, 1/5 in the upper extremities and 3/5 in the hands bilaterally.  Sensation was decreased to light touch in all four extremities. Grade 0 reflexes in bilateral biceps, triceps, patella and ankle.  Downgoing plantar reflex.  Unable to asses gait or perform cerebellar testing secondary to weakness.


Na 137
K >7.0
Cl 100
HCO3 22
BUN 75
Cr 19.4
Glucose 81

Ca 9.8    Mg 2.9
Troponin 0.088
INR 0.9  PT 10.2  PTT 39.3

WBC 9.0
Hgb 9.6
Hct 30.6
Plt 383

JK cxrj

Question #1 Based on your interpretation of the EKG was should you do next?
A)  Place pacer pads on patient in preparation for cardioversion
B)  Give calcium gluconate
C)  Amiodarone 150mg bolus followed by a drip
D)  Activate STEMI pager

Question #2 What other testing should be performed in this patient?
A)  Stat ECHO
B)  Stat EEG
C)  Lumbar puncture
D)  CTA-Head and Neck

Question #3 What immediate intervention needs to be done?
A)  To the OR for aortic dissection repair
B)  Begin treatment with high-dose IVIG
C)  Broad spectrum antiobiotic therapy with Vancomyin, Cefepime and Acyclovir
D)  Emergent Dialysis


Answers & Discussion
This patient presented with a typical presentation for an uncommon disease, Hyperkalemic Paralysis.  Hyperkalemia is a well documented complication in ESRD patients.  They commonly present with cardiac manifestations such as arrhythmias because the cardiac tissue is very sensitive to changes in potassium.  However some patients with severe hyperkalemia have symptoms of muscular paralysis without any cardiac features or EKG changes.  Hyperkalemia has been shown to result in abnormalities of the membrane potential of excitable tissue.   At the cellular level, elevated levels of potassium reduce the transmembrane gradient between intracellular and extracellular compartments leading to partial neuronal depolarization.  The degree of depolarization is directly related the degree of hyperkalemia.  As a result, voltage gated sodium channels are inactivated and these partially depolarized neurons are refractory to excitation leading to muscle weakness.

Question #1 B)
This patients EKG was concerning for hyperkalemia.  He has evidence of peaked T waves, prolonged PR interval with flattened P waves, widened QRS.  You should immediately begin treatment for hyperkalemia, the most important of which is calcium gluconate for cardiac membrane stabilization.  Treatment should also consist of sodium bicarbonate, insulin, glucose, high dose albuterol and kayexalate.

Example of EKG with Hyperkalemia
Figure 2
Patients repeat EKG 2hrs after treatment for Hyperkalemia was started

Question #2 C)
Hyperkalemic paralysis closely mimics Guillan Barré Syndrome; patients present with a rapidly ascending symmetrical paralysis.  Sustained hyperkalemia is thought to exert its effect by impairing the generation of action potentials and increasing the latency of conduction.  Within a few hours of symptom onset the majority of patients are no longer able to walk.  General consensus recommends a lumbar puncture be performed to rule out Guillan Barré.  These two conditions are often unable to be differentiated clinically.  The current recommendation is to perform the lumbar puncture while at the same time treating the patients hyperkalemia.

Question #3 D)
Emergent dialysis is essential for these patients.  Once patients are given treatment for hyperkalemia they should begin to have resolution of their symptoms and after the potassium level is normalized symptoms should completely resolve.  Nerve excitability in patients with chronic renal failure prior to dialysis has shown there are significant abnormalities in axonal excitability in those patients with hyperkalemia.  Axons were depolarized in CRF patients with elevated levels of potassium leading to reduced action potentials and a markedly prolonged relative refractory period.  These abnormalities were significantly and rapidly reduced once serum potassium levels were normalized after dialysis.

Acute ascending paralysis is a rare complication of hyperkalemia but one that is potentially lethal. There have been many conditions associated with hyperkalemic paralysis including Addison’s disease, potassium sparing medications such as TMP-SMX and spironolactone and of course renal failure. My patient refused to have a lumbar puncture performed.  We arranged for him to have emergent dialysis and within 30 minutes of completing dialysis he was up walking around the room asking to go home.  Physicians should have a low threshold for admitting patients with hyperkalemia associated paralysis to an ICU bed as respiratory involvement rapidly leads to respiratory failure.  One must also keep in mind that the use of succinylcholine for rapid-sequence intubation can be fatal to these patients secondary to cardiac arrhythmias.

1.  Cheng CJ, Chiu JS, Huang WH, Lin SH.  Acute hyperkalemic paralysis in a uremic patient.    J Nephrol 2005 16: 630-633.
2.  Gelfan M, Zarate A, Knepshield J.  Geophagia: A Cause of Life-Threatening Hyperkalemia in Patients with Chronic Renal Failure.  JAMA, 1975 234: 738-740.
3.  Hassen GW, Newstead S, Giodano LM.  Hyperkalemic Recurrent Bilateral Lower Extremity Weakness in a Patient on Hemodialysis.  Case Reports in Emergency Medicine 2012.
4.  Kiernan MC, Walters R, Andersen K, Taube D, Murray N, Bostock H.  Nerve excitability changes in chronic renal failure indicate membrane depolarization due to hyperkalaemia.  Brain 2002 125: 1366-1378.
5.  Martinez-Vea, Bardaji A, Garcia C, Oliver JA.  Severe hyperkalemia with minimal electrocardiographic manifestations: a report of seven cases.  J Electrocardiol 1999; 32: 45-9
6.  McCarty M, Jagoda A, Fairweather P.  Hyperkalemic Ascending Paralysis.  Annals of Emergency Medicne 1998 32: 104-107.

VLS 1.2


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