Senior Report 8.19


 Case Presentation by Laura Smylie, MD

A 14 year old girl who presents with nausea and vomiting for one day and an abrupt onset of chest pain.
Vitals: BP 100/67, HR 121, RR 25, Temp 36.7, 100% on room air.




1. What is the diagnosis based upon the above x-rays?
a) Foreign body
b) Pneumothorax
d)Apical pneumonia

2. What is the likely etiology of the radiographic finding?
a) alveolar rupture secondary to forceful retching
b) esophageal rupture secondary to forceful retching
c) acute PE
d) no abnormality on chest x ray.

3. What is the most appropriate initial management of this patient?
a) place on continuous pulse oximetry, place a left sided chest tube
b) place on continuous pulse oximetry, 4mg ondansetron, NPO.
c) place on a continuous cardiac monitor, start heparin drip, consult cardiology.
d) send blood cultures, start antibiotics, encourage PO intake.


Answers and discussion:

1) C
2) A
3) B

1) C – Pneumomediastinum. You can see air tracking in the soft tissues of the neck and the upper aspects of the mediastinum. Although there could potentially be a pneumothorax (B) associated with this this, no pneumothorax can be seen in this study. No foreign body (A) is present and there is no infiltrate to suggest pneumonia (D).



2) A – Alveolar rupture secondary to forceful retching is the most likely etiology of the pneumomediastinum, although you should also be concerned for possible esophageal rupture secondary to forceful wretching (B) also known as Boerhaave’s esophagus. Review of the literature shows that in similar presentations, esophograms are typically negative for tears in the esophagus. Acute PE (C) has not been shown to present with free air. On a chest xray, the most concerning (and classically pimped) findings for acute PE are Hampton’s Hump and Westermark’s sign. Hampton’s Hump, represented in the first image below, shows a wedge shaped area of hyperdensity along the lung parenchyma periphery, indicative of an infact/PE. Westermark’s sign, as shown in the second image below, shows a focal peripheral hyperlucency secondary to oligemia, with or without dilation of the central pulmonary vessels.



3) B – Although there is no obvious pneumothorax on the initial chest x ray, you must keep a high level of suspicion for a small pneumothorax. This would not necessitate chest tube placement (A), but a nonrebreather and continuous pulse oximetry are appropriate if a small pneumothorax is present. Given that the retching led to the pneumomediastinum, treat her nausea with ondansetron. She should be kept NPO until an esophagram can be obtained (as an inpatient or in the observation unit) to definitively rule out Boerhaave’s esophagus. As an inpatient, the chest x ray should repeated in 6-8 hours. C is the treatment for a non-massive PE or NSTEMI; D is the treatment for pneumonia, neither of which applies in this case.


The percentage of pneumothorax will guide therapy. This picture illustrates that 2 cm pneumo is typically the cut off point for inserting a chest tube with a spontaneous pneumo but not necessarily with a traumatic pneumo.




Spontaneous pneumomediastinum: diagnostic and therapeutic interventions. Al-Mufarrej F, Badar J, Gharagozloo F, Tempesta B, Strother E and Margolis M. Journal of Cardiothoracic Surgery 2008, 3:59 doi:10.1186/1749-8090-3-59

BMJ Case Rep. 2012 Oct 10;2012. pii: bcr0320091647. doi: 10.1136/bcr.03.2009.1647.

Gantner J, Keffeler JE, Derr C. Pulmonary embolism: An abdominal pain masquerader. J Emerg Trauma Shock [serial online] 2013 [cited 2015 Mar 26];6:280-2. Available from:

Intern Report 8.14


Case Presented by Brett Sorge, MD

CHIEF COMPLAINT(S): Chest pain and SOB

This is a 67 yo male with HTN, hyperlipidemia and DM who presents with chest pain. His chest pain started this morning (14 hours ago) and is pressure-like and located around the center of his chest. The pain does not radiate, and has not gone away. He is having SOB as well, and feels like he has worse pain with deep breaths. He has had chills since this morning. He has had nausea and vomiting starting today as well. He has had four episodes of non-bloody vomiting total. He admits to a separate epigastric pain as well, that is worse with defecation. The pain does not radiate, and comes and goes. Previous to this morning, he had been tolerating diet with no N/V. He has had pale colored stool ever since a cholecystectomy 3 months ago and has noticed “Vernors”-colored urine. He denies skin changes, itching, or yellowing of his eyes. He denies recent travel, smoking, cough, diarrhea, bright red blood per vomit/rectum, history of cancer or blood clots.

CONSTITUTIONAL: No weight loss.
HEENT: No loss in vision, No runny nose.
SKIN: No rash
GASTROINTESTINAL: No black or bloody stools.
GENITOURINARY: No burning on urination.
MUSCULOSKELETAL: No loss of muscle function.
HEMATOLOGIC: No history of easy bruising.
LYMPHATICS: No history of splenectomy.
PSYCHIATRIC: No history of depression or anxiety.
ENDOCRINE: No polyuria or polydipsia.
ALLERGIES: No history of asthma.

PMD: Patient says he goes to an outside provider for his primary care

PAST MEDICAL HISTORY: Hyperlipidemia, hypertension, diabetes
SURGICAL HISTORY: Cholecystectomy 3 months ago, s/p laparotomy from GSW 30 yrs ago
MEDICATIONS: Patient does not know medications he takes – EMR- metoprolol 50 QD, amlodipine 5 mg QD, losartan 100 QD, atorvastatin 40 QHS, pioglitazone 45 QD
ALLERGIES: Lisinopril
SOCIAL HISTORY: Denies smoking cigarettes, drink alcohol, drug use
FAMILY HISTORY: No family history of early MIs

General: Laying in bed, appears uncomfortable.
Vitals: Blood pressure 215/94, pulse 90, respirations 16, temperature 38.1. Pulse oximetry 100% on room air
HEENT: Head exam was generally normal. No scleral icterus. Mucous membranes were moist.
Cardiovascular: Regular rate and rhythm, no murmurs rubs or gallops
Respiratory: Clear to auscultation bilaterally
Gastrointestinal: Tender to palpation of the epigastric area, soft, non-distended, + BS, multiple scars from previous surgeries
Musculoskeletal: Able to move all extremities
Neurologic: Neurologically, the patient was awake, alert, and oriented to person, place and time. There were no obvious focal neurologic abnormalities. No asterixis or tremor noted.

BMP – 138/3.7/103/25/14/0.86/158 Ca – 9.6
LFT – ALT-724, AST-1637, Alk Phos – 379, t bili – 2.2, d bili – 1.4
Lipase – 63, Ammonia – 69, Lactic Acid – 2.6
CBC – 15.4/13.5/41.7/251
Coags – 23.1, 11.3, 1.06
Troponin – <0.017
EKG – normal
CXR – normal
US RUQ- dilated common bile duct without signs of stone, abscess, or an intra-hepatic process



1. What is the most common symptom in ascending cholangitis?
A. Malaise
B. Jaundice
C. Fever
D. RUQ pain

2. What is the mortality without surgical decompression after 72 hours?
A. 30%
B. 60%
C. 85%
D. 100%

3. Of the answers provided, which antimicrobial therapy is best for empiric therapy for severe cholangitis?
A. azithromycin
B. ceftriaxone
C. ceftriaxone and metronidazole
D. vancomycin

Answers: 1. C, 2. D, 3. C

Many patient’s who present with ascending cholangitis present without classic signs and symptoms.  Classically, patients would present with RUQ pain, fever and jaundice. However, some recent studies have shown that these symptoms may only be present 15-20% of the time. The key symptom is fever, which is present in 90% of patient’s.  Factors that play a role in the pathogenesis of the disease involve an obstruction or an increase in luminal pressure that leads to a bacterial infection.  Risk factors include stones, recent cholecystectomy, ERCP, history of cholangitis, or HIV.  Bacteria are thought to invade the obstructed biliary tree in a retrograde fashion.  The most common bacteria involved are E coli, klebsiella, enterococcus, and bacteroides.  Work-up will show elevated WBC in 79% of patients, with LFT’s indicating cholestasis, with hyperbilirubinemia and an increased alkaline phosphatase level.  The most common sign on ultrasound will be a dilated common bile duct which is only present 64% of the time.  If there is a high clinical suspicion the patient can be taken for ERCP for both diagnosis and therapy.  Empiric anti-microbial therapy should be aimed at treating gram negative, gram positive and anaerobic bacteria. Drainage and decompression are required, with a mortality rate approaching 100% if this is delayed 72 hours.

Intern Report 8.13


Case Presentation by Lauren Kroll, MD

Chief complaint: “I can’t breathe.”

This patient is a 49 year old female with a past medical history of alcohol abuse who presents to the Emergency Department as a medical code for difficulty in breathing. The patient states her difficulty in breathing started gradually last night, and that it is getting progressively worse. She has never experienced anything like this before. She denies fever, chills, cough, congestion, chest pain, and leg swelling. She does admit to some mild epigastric pain, which has been present for the past two days. The epigastric pain is accompanied by nausea and multiple episodes of non-bloody, non-bilious vomiting.

Past medical history: Hypothyroidism, seizure disorder, deep venous thrombosis (diagnosed in December 2014), alcoholism.
Past surgical history: None.
Medications: None (the patient does state she is supposed to be on both levothyroxine and coumadin).
Allergies: Dilantin, phenobarbital.
Social history: Significant for both tobacco and heavy alcohol abuse. No intravenous drug abuse.

Vitals: BP 119/84, HR 126, RR 38, T 35.4, SaO2 99% (room air)

General: Well developed African American female in respiratory distress.

HEENT: Normocephalic, atraumatic. No conjunctival pallor. No scleral icterus. Dry mucous membranes. No pharyngeal erythema. The patient’s breath has a fruity odor.

Cardiovascular: Tachycardic, regular rhythm. No murmurs. No jugular venous distention, no edema.

Respiratory: Tachypnic. Lungs clear to auscultation bilaterally, no wheezes or crackles. No accessory muscle use, no retractions.

Gastrointestinal: Abdomen soft, slightly tender to palpation in the epigastric area, and non-distended. No rebound tenderness, no guarding. Bowel sounds present.

Neurologic: Alert and oriented x 3. Strength equal in all four extremities.

Skin: Warm, dry.

ecg kroll

Laboratory studies:

Basic metabolic panel: Na 137, K 4, Cl 98, HCO3 5, BUN 13, Cr 1.06, glucose 122

Complete blood count: WBC 15.7, Hb 14.2, Hct 43.5, platelets 338

Coagulation studies: PT 10.9, PTT 29.2, INR 1.03

Arterial blood gas: pH 6.879, pCO2 22.1, pO2 95, HCO3 4

Beta-hydroxybutyrate 77.5 (normal 0.2 – 2.8)

Troponin <0.017


Liver function tests: amylase 97, lipase 888, total bilirubin 0.4, direct bilirubin 0.1, ALT 21, AST 68, alkaline phosphatase 98, albumin 2.9

EtOH 151

Urinalysis: 2+ ketones, 2+ protein, specific gravity 1.010, otherwise unremarkable

Chest x-ray:
cxr kroll

The patient’s acid base status is best described as which of the following?
A) anion gap metabolic acidosis (with complete respiratory compensation)
B) non-anion gap metabolic acidosis (with complete respiratory compensation)
C) anion gap metabolic acidosis (with incomplete respiratory compensation)
D) non-anion gap metabolic acidosis (with incomplete respiratory compensation)

2. Initial Emergency Department fluid management for this patient should include which of the following?
A) 5% dextrose in normal saline + insulin
B) 5% dextrose in normal saline + thiamine
C) 5% dextrose in water + thiamine
D) 5% dextrose in water + 3 amps of NaHCO3

3. As the patient is treated in the Emergency Department, which of the following would be expected with repeat blood draws and urinalysis?
A) beta-hydroxybutyrate will decrease; urine ketones will decrease
B) beta-hydroxybutyrate will decrease; urine ketones will remain unchanged
C) beta-hydroxybutyrate will increase then decrease; urine ketones will decrease
D) beta-hydroxybutyrate will decrease; urine ketones will increase then decrease

Answers & Discussion
1) C
2) B
3) D

1. The patient’s acid base status is best described as which of the following?
A) anion gap metabolic acidosis (with complete respiratory compensation)
B) non-anion gap metabolic acidosis (with complete respiratory compensation)
C) anion gap metabolic acidosis (with incomplete respiratory compensation)
D) non-anion gap metabolic acidosis (with incomplete respiratory compensation)

1) In interpreting this patient’s arterial blood gas, we first look at the pH. pH is 6.879; this is an acidosis.

2) Next, in order to determine whether this is a metabolic or a respiratory acidosis, we look at the pCO2. pCO2 is 22.1 (low); therefore, this is a metabolic acidosis.

3) Next, we calculate the patient’s anion gap (anion gap = Na – Cl – HCO3). Anion gap is 34 (high); therefore, this is an anion gap metabolic acidosis. Don’t forget, the patient’s expected anion gap can be determined by multiplying her albumin by three; given her albumin of 2.9, we would expect her anion gap to be approximately 8.7.

4) Next, we can use Winter’s formula (expected pCO2 = 1.5(HCO3) + 8 +/-2) to determine whether or not the patient’s respiratory status is completely compensating for her metabolic derangements. This patient’s expected pCO2 is 15.5, but her actual pCO2 is 22.1; therefore, her respiratory compensation is incomplete.

This patient’s diagnosis is alcoholic ketoacidosis (AKA). Like patients with diabetic ketoacidosis (DKA), those with AKA often also present with nausea and vomiting, which leads to a concomitant metabolic alkalosis. Therefore, it is important to remember that, while the patient’s primary acid base disturbance is an anion gap metabolic acidosis, it is possible for their serum pH to be acidemic, normal, or even alkalemic.

2. Initial Emergency Department fluid management for this patient should include which of the following?
A) 5% dextrose in normal saline + insulin
B) 5% dextrose in normal saline + thiamine
C) 5% dextrose in water + thiamine
D) 5% dextrose in water + 3 amps of NaHCO3

Again, this patient’s diagnosis is alcoholic ketoacidosis (AKA). AKA most commonly occurs in patients who chronically abuse alcohol and abruptly stop drinking; malnutrition and dehydration lead to ketone body formation. Initial Emergency Department management of AKA should include 5% dextrose in normal saline with thiamine added (to prevent Wernicke-Korsakoff Syndrome).

Insulin, although it is an important component of the Emergency Department management of diabetic ketoacidosis (DKA), is contraindicated in the treatment of AKA. Most patients with AKA do not demonstrate hyperglycemia (this patient’s glucose is 122). A bicarbonate drip can be considered in patients with pH < 7.1 (this patient’s pH is 6.879), but is not usually necessary and would not be the first step in managing this patient.

3. As the patient is treated in the Emergency Department, which of the following would be expected with repeat blood draws and urinalysis?
A) beta-hydroxybutyrate will decrease; urine ketones will decrease
B) beta-hydroxybutyrate will decrease; urine ketones will remain unchanged
C) beta-hydroxybutyrate will increase then decrease; urine ketones will decrease
D) beta-hydroxybutyrate will decrease; urine ketones will increase then decrease

In the body, beta-hydroxybutyrate is metabolized to acetoacetate and acetone. Urine dipsticks detect only acetoacetate (not beta-hydroxybutyrate). In alcoholic ketoacidosis (AKA), the initial ratio of beta-hydroxybutyrate to acetoacetate is high. However, as the patient receives treatment, beta-hydroxybutyrate will be metabolized and its serum concentration will decrease. Because beta-hydroxybutyrate is metabolized to acetoacetate and acetone, urine concentrations of acetoacetate (and, thereby, urine ketones) will transiently increase, then decrease.

Teaching Pearls

  1. Suspect alcoholic ketoacidosis in a patient with a history of alcohol abuse who presents to the Emergency Department with an anion gap metabolic acidosis, ketonuria, elevated beta-hydroxybutyrate, and a normal blood glucose.
  1. In addition to an anion gap metabolic acidosis (the primary acid base disturbance in alcoholic ketoacidosis), patients often also present with nausea and vomiting, which leads to a concomitant metabolic alkalosis.
  1. Treatment of alcoholic ketoacidosis includes 5% dextrose in water, with thiamine added. A bicarbonate drip can be used in cases where the patient’s pH is less than 7.1.



Marx JA, Hockberger RS, Walls RM, et al. Rosen’s Emergency Medicine Concepts and Clinical Practice. 8th edition. 2014.

Rosh Review.

UpToDate. Fasting ketosis and alcoholic ketoacidosis. Accessed January 2015.

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

Senior Report 5.21

Case Presentation by Dr. Sarah Albers


“She has got a fever and is throwing up.”


A 16-year-old Caucasian female presents with both of her parents to the emergency department.  The adolescent girl complains of “not feeling well over the past one day.”  She feels dizzy, which she describes further as persistent wooziness that is not positional; there is no sensation that she or the room is spinning. She also feels nauseous, and has a headache – described as a tight band around her temples, with no blurriness of her vision, or change in her vision or hearing. No history of trauma or falls.  She also has generalized myalgias, a sunburn like rash over her trunk, back and upper extremities, redness to her eyes, chills and a fever that started abruptly a couple of hours ago; her temperature was 104 F at home and she took Tylenol, but then vomited it back up.  She states that it hurts her muscles when she takes a deep breath.  She has had no cough or chest pain. She denies shortness of breath or difficulty breathing. No runny nose or sore throat.  No leg pain.  She says she is just feeling “generally weak and my whole body hurts.”

She has had nausea and vomiting today, approximately 10 to 20 episodes of emesis that have been nonbloody, nonbilious.  She has been unable to keep anything down except for a little bit of water and ice chips.  She denies any abdominal pain, blood in her stools, or any black tarry stools.  She states she has bowel movements regularly; her last bowel movement was today with no diarrhea or constipation.  She denies any dysuria, urgency or frequency.  She denies any vaginal discharge, but is currently on her period.

She said she started feeling a little bit “bad” last night with the beginning of a headache; however, today was when everything “hit” her.  She describes as all of these symptoms coming on suddenly.  Mom states she has not been hospitalized nor has she been treated with antibiotics over the past 2 months.  Two months ago she was treated for pneumonia.  She is currently on a homoeopathic medication for Candida called Threelac.  Otherwise, this child is healthy and takes no medications. She has no known sick contacts.


CONSTITUTIONAL:  Positive fever & chills.

EYES:  No change in vision.  Positive red eyes.

ENT:  No change in hearing, runny nose, or sore throat.

RESPIRATORY:  No wheezing, cough, or hemoptysis.

CARDIOVASCULAR:  generalized muscle soreness of her chest wall when taking deep breaths, otherwise no pain.  No palpitations or edema.

GI:  Positive nausea & vomiting.  No diarrhea or constipation.  No black tarry stools or bright red blood per rectum.

GU:  No dysuria, urgency, or frequency.  She is currently on her menstrual cycle.  She does use tampons, and currently has one in.

MUSCULOSKELETAL:  Positive myalgias.  No injury or trauma.

SKIN:  Positive erythematous rash over her trunk, arms, and back.

CNS:  Generalized weakness, no syncope, numbness, speech deficit, confusion or altered mental status.


PAST MEDICAL HISTORY:  None.  However, recent treatment for pneumonia and the patient is currently being treated with a homeopathic medication for a possible candida infection.


MEDICATIONS:  Include a homeopathic called Threelac to treat Candida.  She is also taking a “digestive enzyme”.


FAMILY HISTORY:  negative for hypertension or diabetes

SOCIAL HISTORY:  Negative for tobacco, alcohol, and drugs.  The patient is not currently sexually active.  She has never had sex in the past.  They do have working smoke detectors in the house.  She does always wear a seatbelt in the car.  There are no guns in the house. She does do well in school.


VITAL SIGNS:  On arrival, her blood pressure 111/90, heart rate of 122, respiratory rate is 18, temperature is 39 orally, pulse ox is 95% on room air.

CONSTITUTIONAL AND GENERAL:  The patient is a tall, thin, well-developed, well-nourished female, in no acute respiratory distress, speaking in full sentences, cooperative for exam, A and O x3. She is nontoxic appearing.  She smiles on exam and converses with her parents and me and jokes around a bit. She is sitting upright on the stretcher with her legs drawn up in front of her with her arms wrapped around her legs.  She is wearing a patient gown.  She does have slightly reddened eyes as well as reddish hue to her arms on observation.

HEENT:  Head is normocephalic, atraumatic.  No acute masses or lesions.  Eyes:  Pupils are 3 mm, round and reactive to light.  Extraocular movements are intact.  No conjunctival pallor.  Sclerae are anicteric.  Sclerae are also injected bilaterally.  No evidence of discharge in her eyes.  Nose: no nasal discharge is noted.  Ears:  Tympanic membranes are clear bilaterally. Landmarks are clearly visualized. Mouth and throat:  Mucous membranes are moist.  No erythema, tonsillar exudates or intraoral lesions.

NECK:  Supple.  No lymphadenopathy.  No thyromegaly.  No tenderness to palpation of the cervical spine.  Trachea is midline.  No meningismus or nuchal rigidity.

LUNGS:  Clear to auscultation bilaterally.  No wheezes, rales or rhonchi.  Good air exchange in all lung fields.

HEART:  S1, S2 are present.  Tachycardic rate and regular rhythm, pulses in all four extremities are equal and 2+.

BACK:  No cervical, thoracic, lumbar or sacral spinal tenderness.  The patient has no CVA tenderness.

EXTREMITIES:  No clubbing, cyanosis or edema.

SKIN: The patient does have an erythematous, first degree sunburn-looking rash on the anterior aspect of her bilateral upper extremities as well as her anterior and posterior chest and abdominal wall.  It is blanching in nature.  There are a few very tiny papules on the area of her anterior forearm.  There is no sloughing of skin or bullae formation.  There is no blistering of the skin.  Skin is not tender to touch.  Skin is warm to touch throughout.  She has no erythema or rash on her palms or soles.  She has no rash or erythema on her bilateral lower extremities.

GU:  Performed in the presence of a female nurse chaperone shows normal, Tanner Stage 5, female external genitalia. On speculum exam a tiny amount of blood in the vaginal vault, patient is currently menstruating.  No tampon is present. There is a closed cervical os.  The patient does have pain on insertion of the speculum.  Swabs were obtained. The patient does have cervical motion tenderness as well as bilateral adnexal tenderness. No masses were palpitated. There are no excoriations or sores on the inside of the vaginal vault. Microscopy was negative for trichomonas or clue cells.

NEUROLOGIC:  The patient is awake, alert, and oriented x3.  Normal speech and hearing to finger rub.  Face is symmetrical.  No nystagmus is present.  Sensation is equal and intact throughout.  Motor strength is 5/5 in all four extremities.  The patient does ambulate with a normal gait.


1)    At what point does the accepting hospital assume responsibility for a transfer patient?

  • a.  as soon as the transporting service (ambulance, helicopter) reaches the accepting hospital grounds
  • b.  half-way through transit, when the accepting facility is closer than the  sending facility
  • c.  when the patient arrives inside the accepting facility doors
  • d.  when the patient leaves the sending facility

2)    Which of the following is most likely to predispose a patient to this condition?

  • a.  niacin use
  • b.  recent antibiotic use
  • c.  recent seafood ingestion
  • d.  tampon use

3)    What condition is the patient most likely suffering from?

  • a.  drug-induced dermatitis
  • b.  Stevens-Johnson syndrome
  • c.  toxic epidermal necrolysis
  • d.  toxic shock syndrome


1. d

2. d

3. d (Staph Aureus) Toxic shock syndrome from tampon use


Toxic Shock Syndrome (TSS) is characterized by severe prolonged shock and is caused by a toxin produced by S. Aureus. This was originally described by Todd et al. in 1978.  They reported a series of 7 cases of kids 8-17, S. Aureus was cultured from various body sites, but not the blood, in 5 of the 7 cases.  Most of the subsequent cases have occurred in menstruating females often after a menstrual period associated with tampon use.  In the early 1980’s the consistency of tampons were changed to reduce absorbancy due to growing concerns about TSS.  In the late 1980’s group A Streptococcal toxic shock syndrome (strep TSS) was described because it shares so many feature with TSS.

Menstruation and tampon use is the most common setting for TSS, but non-menstruation TSS accounts for just under half of the reported cases.  Of these cases, strep TSS account for just over half of the cases. Nonmenstrual TSS is associated with super infections of skin including burns, surgical sites, dialysis catheters and lung (influenza associated). It can also happened in association with staph respiratory infections or colonization without an obvious infection source. Strep TSS is classically associated with more severe soft tissue infections including necrotizing fasciitis and myositis, as well as pneumonia, peritonitis, myometritis and osteomyelitis. Mortality reaches 30-70% in strep TSS, and in staph TSS it is <3%.

Staph TSS is caused by the colonization or infection with toxigenic strains, specifically TSST-1 (toxic shock syndrome toxin – 1). Because the organism is not invasive, blood cultures are often negative. Strep TSS is caused by invasive infection with toxigenic strains of GAS (Group A Strep).

The clinical presentation of Strep TSS and staph TSS is similar. The primary difference is that an identifiable source is virtually always present with strep TSS and colonization alone may lead to staph TSS.

Clinical presentation:

Patients may present with fever, chills, nausea, vomiting, diarrhea, headache, myalgias, and pharyngitis.  Prodrome may last hours to 2 or 3 days. The fever is usally high and abrupt in onset (although septic patients may be hypothermic).  The classic rash is a nonpuritic, diffuse, blanching, macular erythroderma.  Initially, this may be mistaken as flushing due to fever.  The rash is typically diffuse but may be localized to the trunk, extremities or perineum.  After about a week a fine flaking desquamation occurs of the face, trunk and extremities followed by full thickness peeling of palms, soles and fingers. This classic rash is much more common with staph TSS and is present in less than 10% of patients with strep TSS.

TSS Rash

Toxic shock syndrome. A. Appearance of the rash associated with staphylococcal toxic shock syndrome (TSS). B. Gangrenous toes associated with prolonged hypotension in TSS. C. Desquamation of the skin that occurs during the resolution of TSS.

The patient’s mental status is frequently abnormal, out of proportion to the hypotension that ensues. Confusion, somnolence, agitiation and combativeness are present in 55% of strep TSS and even more frequent in patients with staph TSS. Other physical findings include pharyngeal and conjunctival erythema, strawberry tongue and peripheral edema. Vaginal mucosal erythema and purulent vaginal discharge may be present in menstrual TSS. As more organ systems become involved a wide range of signs and symptoms may be seen.  GI involvement manifests itself by nausea, vomiting, diarrhea and abdominal pain.  Hepatomegaly may be present. Patients may become hypoxic and develop rales on lung examination.

Comparison for staph and strep TSS

Feature Staph Strep
Age Primarily 15-35 years Primarily 20-50 years
Sex Women > men Women = men
Severe pain Rare Common
Hypotension 100% 100%
Erytheroderma rash Very common Less common
Renal failure Common Common
Bacteremia Low 60%
Tissue necrosis Rare Common
Predisposing factors Tampons, packing, ?NSAID use? Cuts, burns, bruises, varicella, ?NSAID use?
Thrombycytopenia Common Common
Mortality rate 3% 30-70%
  • Risk Factors for TSS
  • tampon use
  • postoperative wound infections
  • postpartum period
  • nasal packing
  • cancer
  • common bacterial infections
  • ETOH abuse
  • infection with influenza A
  • infection with varicella
  • Diabetes
  • HIV
  • Chronic cardiac disease
  • Chronic pulmonary disease
  • NSAID (may mask symptoms rather than be a risk factor)


 The case definition for TSS does not require a positive culture for S. Aureus, but a positive culture is required to diagnose strep TSS. Specific tests are not required to rule out other diseases, but if such tests are obtained the results must be negative.

No specific laboratory changes are associated with TSS, but many abnormalities are common including: leukocytosis or leukopenia, bandemia (very common), elevated creatinine and hemoglobinuria, hypoalbuminemia and hypocalcemia. Other abnormailities include anemia, thrombocytopenia, hyperbilirubinemia, elevated transaminase levels and sterile pyuria.

A lumbar puncture should be performed on febrile patients with altered mental status to evaluate for meningitis. It is prudent to wait for the coagulation profile before the LP, as DIC may exist at the time of presentation. The CSF is normal in TSS.


TSS patients should receive aggressive fluid resuscitation with crystalloids and may require up to 10-20 L a day! Supplemental oxygen should be provided to all septic patients regardless of initial pulse ox. This will allow for maximal tissue oxygenation and reduces acidosis. They should have continuous cardiac and pulse oximetry monitoring.

The source of bacteria (tampons, nasal packs and other foreign bodies) must be removed immediately.  (On our case patient, ROS stated tampon was in and on pelvic exam tampon was out).  Prompt surgical consultation should be obtained to debride wounds. If specimens are sent for culture, the lab should be informed of the suspected diagnosis.

Patients who do not respond to fluids require vasopressors.  Antibiotics (broad spectrum) need to be initiated early in TSS.  Clindamycin is recommended, as it is a potent suppressor of bacterial toxins (dose is 600-900 mg IV q 8h or peds dose is 20-40 mg/kg/day divided every 6-8 hours).


All patients thought to have TSS should be admitted to an ICU!  Again, prompt surgical intervention should be obtained for patients with a wound source.

So back to our patient…

16-year-old adolescent girl presenting with suspected TSS from tampon use.  We had her immediately remove her tampon.  (Note tampon in on ROS, but not during pelvic). On re-evaluation, repeat BP was 70/30-50’s and lab work returned showing:  elevated lactate, acute renal failure, leukocytosis, mild elevation in coags (PT/INR).

ID was consulted and recommended broad spectrum abx including clindamycin, vancomycin and ceftriaxone, which were all started. BP remained at 70’s systolic after 5 L of crystalloid fluids.  Fever and vomiting was controlled with IV NSAIDS and antiemetics.

Patient’s mental status remained AOx3 the entire time, she never looked toxic, continued to smile on exam and wanted to continually walk to the bathroom.  Decision was made to transfer to CHM PICU as a direct admission, CHM requested we not start pressors or a central line at our facility.  They did send PANDA to come get this patient by helicopter.  She ended up on three pressors; dobutamine, Dopamine and vasopressin (all were weaned by hospital day 3) at CHM in the PICU after a femoral line was placed.  Same antibiotics were continued.  Vaginal swab grew Staph Aureus (MSSA), GC and Chlamydia were negative. Blood cultures were negative.  Urine culture grew staph coagulase positive.  After three days in the PICU she was transferred to the ID service and then discharged after one day on the floor.  She was sent out with a 3-week course of clindamycin.  She developed C. Difficile colitis and was treated with oral flagyl and vancomycin.

Intern Report Case Discussion 1.1



A 34-year-old woman presents to the Emergency Department complaining of pain in her right side.  The pain had a gradual onset over the last couple of days.  She first noticed the pain while sitting and watching television. There is nothing that exacerbates the pain.  Pain medication does not provide relief.  Currently the pain is 10/10 and radiates from her right flank to her back and into her pelvis.  She describes the pain as stabbing.  She feels nauseated and had an episode of emesis today.  She denies constipation, diarrhea, fever, chills, chest pain, and shortness of breath.  The patient was evaluated in the ED yesterday for the same pain and was diagnosed with a sexually transmitted disease (STD).  She was started on an antibiotic that she doesn’t have with her.  She was instructed to return to the ED if her pain worsened and was uncontrolled with medication at home.  She returns to the ED with worsening pain.

Physical Exam

VS: BP138/88 mm Hg    HR70 beats per minute  RR 18 breaths per minute  Temp 36.5°C, and oxygen saturation of 99% on room air.

General appearance: writhing around on the stretcher, holding her right side, periodically tearful

Head: atraumatic

Eyes: EOMI, PERRLA, anicteric, no pallor

Mouth: mucosa moist, normal tonsils without erythema, vesicles, or exudates

Neck: supple, no lymphadenopathy, no JVD, no goiter

Respiratory: CTA b/l, no wheezes, rales, or rhonchi

Cardiovascular: no murmurs, rubs, or gallops, 2+ pulses in all extremities

Abdomen: obese, soft, tender in the right upper and lower quadrants, no rebound or guarding, mild CVA tenderness on the right, normal bowel sounds

Pelvic: whitish foul-smelling discharge, os is closed, friable cervix with minimal bleeding when swab taken, no cervical motion tenderness

Extremities: no cyanosis, clubbing, or edema

Musculoskeletal: full range of motion throughout

Skin: warm and dry, no rashes

Neurological: A & O x3, CN II-XII intact, normal sensation and strength throughout
Lab Results

CBC and electrolytes within normal limits

U/A: 2-5 trichomonas, trace leukocyte esterase, no nitrites, no blood, 2+ bacteria

Diagnostic Studies

CT Abdomen-Pelvis w/o contrast: 2 cm hypodense mass in left adrenal gland, 4.4 cm cyst in left adnexa, 6.1 cm cyst in right adnexa, gallbladder, kidneys, and appendix all normal in appearance
Pelvic U/S: left ovary is 5×4×3 cm, right ovary is 7×5x5cm containing a 3×4x4cm hypoechoic lesion with no arterial wave form, fluid in the right cul-de-sac


1. What is the most common type of adnexal mass in the reproductive years?
A.    fibroid
B.    tubo-ovarian abscess
C.    carcinoma
D.    physiologic cyst
E.    endometrioma

2. What is the first step in management of a woman with pelvic pain and unstable vital signs?
A.    consult to Ob/Gyn
B.    send to OR
C.    wide-bore IV access and volume resuscitation
D.    CBC and electrolytes
E.    Pelvic ultrasound

3. What is the gold standard for diagnosis of acute pelvic pathology?
A.    ultrasound
B.    laparoscopy
C.    laboratory tests
D.    CT with contrast
E.    CT without contrast


Summary: A 34-year-old woman presents to the Emergency Department complaining of pain in her right side, gradually worsening over the last couple of days.  Diagnostic scans assisted in the identification of ovarian torsion with complete lack of blood flow to the right ovary.  The patient was brought to the operating room for a diagnostic laparoscopy.  The right ovary and tube were found to be torsed four times with a 6 cm hemorrhagic cyst on the ovary.  After untwisting the adnexa, blood flow was not normalized.  Surgeons proceeded with a right oophorectomy.  The patient tolerated the procedure well and was discharged home from the recovery room.

The differential diagnosis of abdominal pain is extremely broad.  Even if the differential is limited to pelvic pathology there are still numerous causes that could be disastrous.  As always, we begin with the history and physical in order to give us an idea of where the pain might be coming from.  The patient in this case was an atypical presentation for ovarian torsion, in that her pain was more in the flank with radiation to the back and pelvis, as well as the fact that her pain was more of a gradual onset.  A more typical presentation would involve acute onset of pain that is more localized in the pelvic area with lateralization to the affected side.  However, because torsion can be intermittent, pain may still not be constantly present.

As is the case with any patient presenting to the Emergency Department, immediate life threats must first be ruled out, and this is typically based on the patient’s vital signs and overall clinical picture.  With our patient, although she was clearly in distress, her vital signs were stable and remained so.  In addition, she did not have peritoneal signs suggestive of a ruptured viscous or inflammation.  Had our patient been unstable a resuscitative approach involving wide-bore IV access, fluid boluses, supplemental oxygen, and cardiac monitoring would have been appropriate.  As that was not the case, the standard approach for a patient with pelvic pain in the ED involves a urine pregnancy test, urinalysis, and pelvic exam.  This assists in the diagnosis of many forms of pathology.  This can be supplemented by basic labs including CBC and electrolytes.

As none of this was diagnostic in our patient, the next step was to move onto imaging.  Given a history of flank pain with radiation to the back and pelvis, a CT scan is a highly sensitive and specific test to check for both nephrolithiasis and appendicitis.  What we found was that the patient had a large cyst on her right ovary, without pathology in the appendix, gallbladder, or kidney.  This lead to the final imaging test, ultrasound with Doppler, which gave us our tentative diagnosis of ovarian torsion.  The confirmatory test, which was both diagnostic and therapeutic, was laparoscopy.


1. D. During the reproductive years the ovaries produce a dominant follicle in the first half of the menstrual cycle and a corpus luteum after ovulation.  Either structure can become fluid-filled and enlarged, producing a physiologic cyst.  This is the most common form of adnexal mass at this point in the patient’s life.  Fibroids do not form in the adnexa.  TOA, carcinoma, and endometrioma are possible causes of an adnexal mass, but given that a physiologic cyst can form twice a month they are not as likely to be the diagnosis.
2. C. Vital signs are vital.  The first step in management of any patient presenting to the ED with unstable vitals requires aggressive volume resuscitation.  A stat OB/GYN or surgery consult would then be sought if the history or physical exam is suggestive of a pelvic pathology.  Persistent shock would necessitate operative management next, but if the patient stabilizes, a pelvic ultrasound or CT should be used to identify the cause of the problem.  Lab tests are only used in the stable patient, and a pregnancy screen and U/A will provide more information in a patient with pelvic pain than a CBC and electrolytes.
3. B. Laparoscopy is considered the gold standard for diagnosing pelvic pathology.  Like so many other gold standard tests for other pathological processes, it is invasive and therefore not commonly used as the initial diagnostic modality. Ultrasound and CT are often used first and can frequently make the diagnosis in order to avoid an invasive procedure, but laparoscopy is still necessary when the diagnosis is unclear, or when immediate definitive treatment is required.  In addition, CT scan sometimes requires the injection if IV contrast that can lead to nephropathy.  Radiation exposure should also be taken into consideration.  Lab tests will aid in the diagnosis of infection or electrolyte imbalance in a patient with vomiting, like ours, but cannot ultimately make the diagnosis by themselves.



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Chang HC, Bhatt S, Dogra VS. “Pearls and pitfalls in diagnosis of ovarian torsion.” Radiographics. 2008 Sep-Oct;28(5):1355-68.

Lo LM, Chang SD, Horng SG, Yang TY, Lee CL, Liang CC. “Laparoscopy versus laparotomy for surgical intervention of ovarian torsion.” J Obstet Gynaecol Res. 2008 Dec;34(6):1020-5.

Marx John et al. Rosen’t Emergency Medicine. Philadelphia: 2006, pp248-253.

Vandermeer FQ, Wong-You-Cheong JJ. “Imaging of acute pelvic pain” Clin Obstet Gynecol. 2009 Mar;52(1):2-20.

This case discussion presented by Brian Kern, MD.