Senior Report 8.21


Case Presentation by Dr. Sean Michael, MD

Visual Stimulus Case:

A 59-year-old man with COPD presents with acute dyspnea. His breath sounds are nearly inaudible. He is tripoding with accessory muscle use and suprasternal retractions. Temperature is 37.7°C, heart rate 112, respiratory rate 36, blood pressure 168/92, and oxygen saturation 89% on 2 liters via nasal cannula. Glucocorticoids and nebulized bronchodilators are administered. Bedside thoracic ultrasound is performed and demonstrates the following M-mode image in the right second intercostal space:



  1. The most likely etiology of the ultrasonographic finding above is:

A. Emphysematous bulla or apical bleb

B. Iatrogenic pneumothorax

C. Lobar pneumonia

D. Primary spontaneous pneumothorax


Additional images are obtained of the right chest at the level of the fifth intercostal space:





  1. Given the new information obtained in this image, which of the following is the best course of action:

A. CT Thorax

B. Intravenous antibiotics

C. Non-invasive positive pressure ventilation

D. Tube thoracostomy


  1. The findings in the second ultrasound image serve mostly to:

A. Increase diagnostic sensitivity (ie. have a high negative predictive value)

B. Increase diagnostic specificity (ie. have a high positive predictive value)

C. Predict a decreased risk of mortality

D. Predict an increased risk of treatment failure


Answers and explanation:

1. A
2. D
3. B

(Note: This explanation assumes that you understand the basics of lung ultrasound. If you need a refresher, there are lots of great online resources.)

This patient presented with an apparent moderate to severe COPD exacerbation with hypoxia and poor air exchange on lung auscultation. Bedside lung ultrasound (image 1) demonstrates absence of pleural sliding on M-mode. In the setting of COPD (or many other critical illness states), the absence of lung sliding may be caused by any number of pathophysiologic conditions. While the absence of lung sliding is quite sensitive for pneumothorax of any etiology, in comparison to patients with traumatic pneumothorax, patients with non-traumatic dyspnea may have numerous other causes of poor lung sliding, which may increase the false-positive rate for ultrasound exams (Slater 2006, Lichtenstein 2008).

In this clinical presentation, the most likely reason for the absence of lung sliding is an emphysematous bulla/apical bleb (question 1, answer A). Bullae are common in COPD, especially in advanced disease, and a ruptured apical bleb is a common cause of secondary spontaneous pneumothorax (Noppen 2008). While iatrogenic pneumothorax (question 1, answer B) is a known complication of a number of procedures, this patient did not undergo any high-risk interventions, such as transthoracic needle aspiration, central venous access, thoracentesis, transbronchial or pleural biopsy, or positive pressure ventilation (Sassoon 1992). Lobar pneumonia (question 1, answer C) on ultrasound is characterized mostly by an A-B profile or by the absence of lung sliding with a B profile (Lichtenstein 2008). Primary spontaneous pneumothorax (question 1, answer D) typically occurs in young male smokers with thin body habitus and (by definition) is not secondary to underlying pulmonary disease, such as COPD, cystic fibrosis, or malignancy (Noppen 2008).

The second ultrasound image shows a lung point, which is much more specific for pneumothorax (Lichtenstein 2008). Given the patient’s dyspnea, hypoxia, and the size of the pneumothorax (from at least the second through the fifth intercostal spaces, but more likely from the apex through the fifth), the correct intervention is tube thoracostomy (question 2, answer D). This can be accomplished with either a small bore surgical chest tube or via percutaneous small-bore catheter (aka “a pigtail”) (Contou 2012, Tsai 2006). There is already enough clinical information to diagnose pneumothorax, and CT Thorax (question 2, answer A) is not required. Intravenous antibiotics (question 2, answer B) might be indicated in suspected bacterial pneumonia, but the second ultrasound image is not diagnostic of pneumonia. Non-invasive positive pressure ventilation (question 2, answer C) may be required for this patient, which is an even more compelling reason to perform thoracostomy. The ultrasound does not predict need for NIPPV, however.

As mentioned previously, lung point dramatically increases specificity (question 3, answer B) for pneumothorax (Lichtenstein 2008 and lots of other papers—this isn’t a comprehensive review). The most sensitive (question 3, answer A) finding is absence of lung sliding (or perhaps absence of sliding with augmented color power Doppler) (Cunningham 2002, Lichtenstein 2008, etc). Lung ultrasound has not yet been shown to predict either treatment failure (question 3, answer C) or mortality (question 3, answer D) in the setting of secondary spontaneous pneumothorax.

In this case, a small-bore chest tube was placed, the patient placed on bi-level NIPPV, and he did well.


Contou D, Razazi K, Katsahian S, et al. Small-bore catheter versus chest tube drainage for pneumothorax. American Journal of Emergency Medicine. 2012;30(8):1407–1413. doi:10.1016/j.ajem.2011.10.014.
Cunningham J, Kirkpatrick AW, Nicolaou S, et al. Enhanced recognition of “lung sliding” with power color Doppler imaging in the diagnosis of pneumothorax. J Trauma. 2002;52(4):769–771.
Lichtenstein DA. Relevance of Lung Ultrasound in the Diagnosis of Acute Respiratory Failure*. Chest. 2008;134(1):117. doi:10.1378/chest.07-2800.
Noppen M, De Keukeleire T. Pneumothorax. Respiration. 2008;76(2):121–127. doi:10.1159/000135932.
Sassoon CS, Light RW, OHara VS, Moritz TE. Iatrogenic pneumothorax: etiology and morbidity. Respiration. 1992;4:215–20.
Slater A, Goodwin M, Anderson KE, Gleeson FV. COPD can mimic the appearance of pneumothorax on thoracic ultrasound. Chest. 2006;129(3):545–550. doi:10.1378/chest.129.3.545.
Tsai W-K, Chen W, Lee J-C, et al. Pigtail catheters vs large-bore chest tubes for management of secondary spontaneous pneumothoraces in adults. The American journal of emergency medicine. 2006;24(7):795–800. doi:10.1016/j.ajem.2006.04.006.
Ultrasound for Detection of Pneumothorax. Rebel EM ( Accessed 3/20/2015.

Intern Report 8.20


Case Presentation by Khoa Nguyen, MD

CC: “fever and runny nose”


HPI: 9-day-old full term female born via C-section who presents with cough, rhinorrhea, and tactile fever. Patient’s mother stated that the patient had rhinorrhea 3 days ago who then developed a cough the following day. The mother then felt that the patient was warm in the back but did not measure any temperature. The patient was not given any anti-pyretic or antibiotics. There had been green discharges from the eyes. Patient had 2 episodes of non-bloody nonbilious emesis that looked like her feeds. Patient had been sleeping more than normal. On further questioning, the patient’s mother had GBS and Chlamydia with this pregnancy and had HSV during the previous pregnancy.   There were no changes in the number of wet diapers and no changes in PO intake.



Constitutional: positive for tactile fever

HEENT: positive for rhinorrhea, green discharges from eyes, and congestion

CV: neg

Pulmonary: positive for coughing

GI: positive for 2 episodes of NBNB emesis. No changes in appetite and PO intake.

GU: no change in number of wet diapers

The rest of the ROS were negative


PMH/PSH: none

Allergies: NKDA

Immunizations: UTD

Birth history: 39 wks, repeat c-section

Family history: Mother was treated for GBS and chlamydia with this pregnancy


Physical Exam:

Vital signs: Temperature 37, HR 160, RR 30, BP 67/41, 98% on RA

General: patient is alert and responsive to touch

HEENT: NC/AT, anterior fontanelle is open, soft, and flat. There is bilateral eye discharge with crusting. No chemosis. Eyelids appear normal. TMs are clear. Oropharynx within normal limits

Neck: supple

CV: RRR, S1 S2, no notable murmurs

Lung: Clear to auscultation bilaterally

GI: soft, nontender, non distended, no masses

MSK: moving all extremities

Skin: no rashes, bruising

Neuro: normal moro, rooting, grasp



  1. What is the workup for this patient?

A. Patient does not need a workup.

B. Full sepsis workup: LP, CBC, CXR, LP, UA with culture, blood culture, RSV/Flu.

C. UA with culture, CBC, Chest x-ray

D. Rapid Viral antigen testing


  1. What is the management?

A. PO challenge and discharge home after reassuring the mother that this is likely a viral infection and that she needs to follow-up with PMD.

B. Ampicillin, ceftriaxone, and acyclovir

C. Ampicillin and acyclovir

D. Ampicillin, cefotaxime, and acyclovir


  1. Which of the following is true?

A. Management of pediatric fever is the same throughout all ages.

B. Defervescence after acetaminophen administration has been shown to reliably exclude bacteremia in children of any ages.

C. The absence of fever does not eliminate the possibility of serious bacterial illness.

D. A thorough history and physical exam can exclude a serious bacterial illness in a patient less than 28 days old.



1. B
2. D
3. C


Pediatric patients from 0-28 days of age who present with a fever are at a high risk for bacterial illness. Fever may be the only clinical manifestation of a potentially life-threatening disease. However, in this age group, the absence of fever does NOT eliminate the possibility of serious bacterial illness because more than half of neonates with meningitis are afebrile.

The physical exam in this age group is insensitive to exclude serious bacterial illness.

Here are some of the findings to suggest bacterial meningitis:

Vital signs – apnea, tachypnea, hypothermia, hyperthermia, bradycardia, tachycardia. The absence of fever does not rule out the possibility of serious bacterial illness.
Behavior – listless, restless, irritable, lethargy, change in sleeping pattern
Neurologic – high pitch cry, nystagmus, vacant stare, seizure, altered tone, absence of cry
Dermatologic – cyanosis, petechiae, purpura, livedo reticularis
GI – altered feeding, diarrhea, vomiting, abdominal distention, jaundice


B – Although the patient has symptoms to suggest a viral infection, she needs a thorough workup given her age. A change in sleeping pattern, cough, eye discharges, and tactile fever must be taken seriously. Additionally, the patient’s mother has a history of GBS, chlamydia, and HSV which all put the patient at risk of a serious infection. For these reasons, the patient needs a complete sepsis evaluation.
D – The patient should be treated empirically with broad spectrum medications in the ED given her risks of a serious infection. Ceftriaxone should be avoided in patients younger than 28 days because of a hypothetical risk of causing bilirubin encephalopathy since this medication causes bilirubin to be displaced from protein binding sites.
C – Management of pediatric fever depends on the age of the patient. Defervescence of a fever after Tylenol ingestion does not exclude bacteremia in children of any ages.



Marx, JA, Hockerberger R, Walls RM. Rosen’s Emergency Medicine: Concepts and Clinical Practice (8th edition), Mosby 2013.

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:

Senior Report 8.18


 Case Discussion by Erin Ge, MD


CC: “Nausea”


This is an 80 year old female who presents with nausea. She states she has been feeling nauseated and generally unwell for the past week. She denies any significant abdominal pain, vomiting or diarrhea. She has not had any fevers or chills. She reports feeling like she has no energy. She has been refusing to eat. Her family states she has seemed progressively more confused and has been “seeing double”. Today, she started complaining of some episodes of “heart racing” so her family brought her in for evaluation. She denies chest pain or shortness of breath.


General: Positive for generalized weakness

Neurological: Positive for confusion

Ear, Nose and Throat: No congestion

Eyes: Positive for diplopia

Cardiovascular: Positive for palpitations

Pulmonary: No shortness of breath

Abdomen: See HPI

Genitourinary: No polyuria

Musculoskeletal: No back pain

Skin: No rashes


Past Medical History: Congestive heart failure, hypertension, coronary artery disease

Past Surgical History: Cardiac catheterization, total hysterectomy

Family History: Hypertension

Social History: Lives with her daughter, history of tobacco use but quit over 20 years ago, denies alcohol or illicit drug use

Medications: Aspirin, Lisinopril, Lasix, digoxin, omeprazole

Allergies: NKDA


Physical Exam:

General: Overweight, nontoxic

Vitals: Blood pressure 125/92, heart rate 80, respiratory rate 16, temperature 36.8, pulse oximetry 98% on room air

HENT: Normocephalic, atraumatic, mucous membranes moist, trachea midline

Eyes: Sclerae noninjected and nonicteric, pupils 3mm, equal, round and reactive to light, EOMI

Cardiovascular: rate and rhythm regular, normal S1, S2, no murmurs, no JVD, 1+ bilateral lower extremity edema

Respiratory: Clear to auscultation bilaterally with good air entry and equal chest rise

Gastrointestinal: Soft, nontender, non distended, no rebound tenderness, negative Murphy sign, no CVA tenderness

Musculoskeletal: No obvious deformities, extremities nontender, moves all extremities equally

Skin: No erythema, rashes or ulcerations

Neurologic: Alert, oriented x 3, responds slowly, no facial asymmetry, no speech dysarthria, sensation intact to light touch bilateral upper and lower extremities, 5/5 strength bilateral upper and lower extremities





Laboratory Studies:

CBG – 97


5.1           12.0        122



138         97            24            103

6.0           20            2.1

Troponin <0.017

SDS: neg

UDS: neg

Digoxin level: 4.0 ng/mL (nml 0.5-2.0)



1. In the initial management of an acute digoxin overdose, which of the following should be considered:

A. Gastric lavage

B. Emergent dialysis

C. Activated charcoal

D. High dose insulin


2. You are informed by nursing staff that the patient is now tachycardic and a new EKG is obtained:


What next intervention is indicated?

A. Lidocaine

B. Transvenous pacing

C. Quinidine

D. Procainamide


3. What is the appropriate treatment for this patient’s hyperkalemia?

A. Insulin/glucose, sodium bicarbonate, calcium gluconate and kayexalate

B. Fab fragments

C. Emergent dialysis

D. Isotonic fluid hydration



1. c

2. a

3. b

Digoxin toxicity typically presents with nonspecific symptoms. Generalized weakness, nausea and decreased appetite are often reported.  Visual symptoms are also often seen with the classic being xanthopsia where patients describe yellow halos around lights (think van Gogh’s Starry Night) or other distortions in colors particularly yellow and green. Cardiac dysrhythmias are also typical and the life threatening complications of this overdose.  The patient’s initial EKG should lead the clinician to be suspicious of a dig overdose even prior to receiving the elevated level. The “scooped” appearance of the ST segment or the so called “Salvador Dali” moustache indicates use of digoxin (NOT toxicity).  The multiple PVCs should increase a clinician’s suspicion for toxicity as this is the most common early sign.

1.    The correct answer is C. Activated charcoal.  This can prevent systemic absorption of the drug, although more likely useful in an acute overdose as opposed to a chronic.  Gastric lavage (a.) is contraindicated in this overdose as it can lead to increased vagal stimulation which can produce fatal arrhythmias in this patient.  Emergent dialysis (b.) is also incorrect as digoxin has a wide nonvascular distribution and therefore dialysis does not effectively remove a significant amount of the drug.  High dose insulin is used to treat beta blocker and calcium channel blocker overdoses and does not have a role in digoxin overdose.

2.   A. One the classic (and terrifying looking!) arrhythmias which may be induced by dig toxicity is bidirectional ventricular tachycardia which is demonstrated in the EKG.  The QRS complex axis shifts 180 degrees with each beat (see green arrows).  This is a rare tachyarrhythmia, but classically associated with dig toxicity.  Lidocaine (a.) is the correct answer and has been shown to effectively treat this arrhythmia along with phenytoin. Pacing (b.) or cardioversion should be avoided if possible as they can induce worsening dysrhythmias and if used, low energies are to be used. Both quinidine (c.) and procainamide (d.) are class IA antidysrhythmics and can lead to worsening of the arrhythmia. Quinidine, in particular, has been shown to increase levels of digoxin and therefore worsen toxicity.

3.   B.  The treatment of hyperkalemia in the setting of dig toxicity is treatment of the toxicity itself with administration of digoxin immune Fab (b.). The hyperkalemia itself in this patient would be an indication for use of this, but also the significant dysrhythmia would obviously be another indication. Traditional hyperkalemia treatment (a.) can be used with the exception of calcium.  The “stone heart” theory is the reason calcium in contraindicated in these patients.  Dig toxicity itself causes an elevation of the intracellular calcium concentration and the theory states that further increases in calcium can lead to a “stone heart” or an irreversible noncontractile state.  This is based on case reports and recent studies show evidence that this is likely a false theory, however, the board exam answer is still to avoid calcium in these patients (sorry). Neither emergent dialysis (c.) or IV fluid hydration (d.) are significantly effective in reducing dig levels which is the underlying cause of the hyperkalemia.

As a side note, hyperkalemia is more likely in an acute ingestion (think healthy toddler who got into Grandma’s meds), and less likely in this patient who fits a chronic ingestion picture (known history of taking this medication, potentially induced by decreased renal clearance with an elevated creatinine, although baseline is unknown).


Cadogan, Mike, and Nickson Chris. “Life in the FastLane.” Web.

Goldfrank, Lewis R. Goldfrank’s Toxicologic Emergencies. New York: McGraw-Hill Medical Pub. Division, 2002.

“Hippo EM.” Emergency Medicine Board Review, LLSA, & More. Web. <;

 Mahadevan, Swaminatha V., and Gus M. Garmel. An Introduction to Clinical Emergency Medicine. Cambridge: Cambridge UP, 2005.

Marx, John A., Robert S. Hockberger, Ron M. Walls, James Adams, and Peter Rosen. “Cardiovascular Drugs.” Rosen’s Emergency Medicine: Concepts and Clinical Practice. Philadelphia: Mosby/Elsevier, 2010.

Intern Report 8.17


Case Presented by Jeff Butler, MD

Chief Complaint: abdominal pain, diarrhea, weakness

HPI: An otherwise healthy 6yo boy presents with three days of abdominal pain, nausea, vomiting, and diarrhea. His symptoms started with nausea and vomiting, and were followed by fever and epigastric, cramping abdominal pain. By Day 2 of his illness he was having frequent loose stools up to 15 times per day. The mother decided to bring the child in after he developed some weakness and difficulty walking prior to arrival. The vomiting occurred around 2-4 times per day and was characterized as nonbloody and nonbilious. There was also no blood noted in the stool. The child has had a poor appetite in the last two days and has been refusing meals after two episodes of post-prandial emesis. The mother thinks the child may have been urinating less frequently since this morning. The fever is being treated with alternating motrin and Tylenol last given 2 hours prior to arrival. The child had multiple sick contacts with similar symptoms at daycare and there was no history of recent travel.

Constitution: positive for fevers, negative for weight change
HEENT: negative for ear pain, sore throat
Cardiac: negative for chest pain, palpitations
Pulm: negative for wheezing, cough
GI: positive for abd pain, diarrhea, vomiting
GU: positive for decreased urination
MSK: negative for joint pain, swelling, myalgia, positive for weakness
Neuro: positive for dizziness, HA

PMHX: none

PSHx: none

Allergies: NKDA

Meds: Motrin, Tylenol PRN fever

SocHx: no tobacco use in the home, patient attends school and daycare, lives with mom, dad, two brothers.

Vitals: T37.1, HR140, BP100/60, R20, SpO2 99% RA
General: Ill-appearing male child sitting on the exam table in mild distress due to weakness
Eyes: PERRL, EOM, no pallor
HENT: Normal tympanic membrane without erythema or purulent drainage, dry oral mucous membranes, neck supple and nontender without LAD
CV: Tachycardic regular rate with normal hearts sounds, pulses 2+ at radial and dorsalis pedis bilaterally, cap refill 2 seconds
Pulm: Normal work of breathing with clear breath sounds bilaterally
Abd: Soft, mildly tender to palpation over epigastrium, no rebound tenderness or guarding, normoactive bowel sounds
Skin: No rashes, bruises, or petechiae
Neuro: Normal mentation, no facial droop, tongue midleine, smiles symmetrically, 4/5 strength with hip flexion bilaterally, 4/5 strength with leg flexion and extension bilaterally, 5/5 strength otherwise throughout, sensation intact to light touch throughout, no clonus

You begin IV hydration with a 20cc/kg bolus and start weight-based maintenance fluids. Lab tests were ordered as follows:

WBC- 9.4
Hgb- 13.5
Plts- 278

Na- 134
Cl- 105
K- 1.9
HCO3- 19
BUN- 20
Cr- 1.1
Glu- 89

Q1. Which of the following is a spurious cause of hypokalemia?
A) Recent fluid administration in the IV site
B) Sample deterioration
C) Hemolysis
D) Cold storage

Q2. What EKG finding can be found with hypokalemia?
A) Peaked T waves
B) U waves
C) J waves
D) QRS prolongation

Q3. What is the best method for replacing this patient’s electrolyte abnormalities?
A) No replacement needed
B) PO potassium
C) IV potassium
D) Yes, supplement with magnesium and IV potassium

Bonus Question:
Q4. What is the most likely acid-base disorder this patient will have? Maybe make this the bonus questions but clinically not as important as the next question
A) Respiratory acidosis
B) Metabolic alkalosis
C) AG metabolic acidosis
D) NAG metabolic acidosis


Answers: 1. A, 2. B, 3. D, 4. D


There are a couple important causes of spurious hypokalemia, most of which will be due to elements outside of your control except by thinking ahead and, for example, asking nursing staff to hold IV fluids before drawing labs. If you think the hypokalemia is spurious due to white cell consumption as in the case of the high leukocytosis usually associated with sepsis or leukemia you can call the lab and try to determine whether there were delays in analysis.
However, if the hypokalemia is clinically significant such that you suspect the need for IV supplementation you may be able to quickly verify the result based on EKG findings that include flattened T waves and U waves. Peaked T waves and QRS prolongation are more typical of hyperkalemia.
For a potassium > 2.5 mmol/L it is appropriate to replete with an oral dose of 0.5 mmol/kg for kids age < 5, and 1 mmol/kg in younger kids. However, repletion of severe hypokalemia is complicated by the fact that potassium is an irritant to peripheral veins and higher IV doses result in transiently increased cardiac concentrations that can cause cardiac arrest. This patient will likely require ICU admission for potassium repletion, cardiac monitoring, and q4-6h electrolyte checks where it will be appropriate to calculate a total body potassium deficit but a dose of 0.3 mmol/kg/h can be started in the ED through a peripheral vein. Magnesium should also be supplemented because depletion often coexists with hypokalemia, low magnesium impairs renal potassium reabsorption, and patients are at higher risk for a ventricular arrhythmia as described below.
Diarrheal stool contains a relatively high potassium content and diarrhea is the main cause of hypokalemia worldwide. The stool also contains a significant amount of bicarb, the loss of which is adjusted for by the kidneys with the H+/K+ antiporter, exchanging intracellular potassium for extracellular protons. Thus, the sufficient loss of bicarbonate ionically balanced through shifts in potassium result in a non-anion gap metabolic acidosis. The low serum potassium in the setting of this regulatory mechanism by the kidneys indicates an even more profound degree of total body potassium loss that should prompt repletion. Clinically, hypokalemia is most likely to affect the heart and muscles with severe cases of hypokalemia (< 2.5 mmol/L) resulting in complete muscle paralysis, rhabdomyolysis, and torsades or ventricular fibrillation. However, hypokalemia by itself rarely causes the cardiac complications just mentioned, and instead potentiate other causes of these like hypomagnesemia.
Marx, JA, Hockerberger R, Walls RM. Rosen’s Emergency Medicine: Concepts and Clinical Practice (8th edition), Mosby 2013.

Nickson, C. Life in the Fast Lane ( 2010.

Welfare, W, Sasi P, English M. Challenges in managing profound hypokalmia. BMJ. 2002. Feb 2; 324(7332): 269-70.

Intern Report 8.16


Case Discussion presented by Wissam Rhayem, MD


Chief Complaint:  “Chest Pain”

History of Present Illness:

This is a 26 y/o male prisoner presenting with a chief complaint of chest pain and palpitations.

The patient has a history of Wolff-Parkinson-White and poly-substance abuse. He states that he takes 20-40 mg of Xanax daily along with any Ativan, Klonopin, and Seroquel that he can obtain. The story is unclear, but the patient claims that he has been taking Xanax while in prison. The patient has been in prison for the last 9 days. He denies nausea, vomiting, headache, diarrhea, constipation, visual changes, fever, chills, or difficulty breathing.

Medications: Xanax 20-40 mg daily; Ativan; Klonopin; Seroquel; none are prescription

PMH: Wolff-Parkinson-White

Social History: + cannabis; + cigarettes; + alcohol weekly


Physical Exam:

VITALS: BP 127/80 HR 104 bpm T 36.1°C RR 16 bpm SpO2 98%

General: severe distress; agitated; not oriented

HEENT: pupils 3 mm; PERRL; EOMI; atraumatic

CV: regular rate and rhythm; no murmurs, rubs, or gallops

Pulmonary: breath sounds are clear bilaterally without rales, rhonchi or wheezing.

GI: soft, nontender, nondistended; no palpable masses

Musculoskeletal: no deformity; full ROM in all four extremities

Skin: no cyanosis; good perfusion in all four extremities; palpable pulses in all extremities

Neuro: not oriented; uncooperative; no focal deficits; normal deep tendon reflexes

Psych: uncooperative; agitated; labile mood; hostile; belligerent; pressured speech


EKG: no delta wave; shortened PR interval; normal sinus rhythm

BMP: Na 139; K 4.0; Cl 104; CO2 30; BUN 11; Creatinine 0.99; Glucose 117

CBC: WBC 9.1; HgB 14.7; Hct 44.2; Plt 220

UDS: + BZDA; + cannabinoids

TROP: < 0.017 x 2


Medical Course:

While the patient is waiting for transfer to CDU,  his mental status begins to deteriorate. Now at 24 hours after initial presentation, he starts having visual hallucinations and becoming very agitated and delirious. He is demanding “footballs” and “candy bars.” The patient is screaming and is very verbally abusive. He is tugging violently at his restraints and is fighting to get out of bed. He does not respond to an initial 10 mg of IV Valium (diazepam). He is then given 10 mg, then 20 mg, then 40 mg, then 80 mg of IV Valium, each 5 minutes apart, until light sedation is achieved. At this point, he reports that his chest pain has resolved.

After about 90 minutes of sleep the patient sits straight up in bed, screaming for a urinal. The patient is now tachycardic and hypertensive. He is given a urinal and voids 900 mL of urine. Tachycardia and hypertension immediately resolve. He is noted to have tongue fasciculations and hand tremors at this time. He starts to become extremely agitated again and is given 20 mg, then 40 mg, then 80 mg, and then 160 mg of IV Valium each 5 minutes apart until he sleeps. A foley is placed to avoid further urinary retention.

Hospital pharmacy warns that they are running out of Valium. A propofol drip is then started. In the process of starting the drip, the patient becomes agitated again and requires 40 mg of IV Valium, followed by another 40 mg of IV Valium 5 minutes later. The drip is started at 20 mcg/kg/min. The patient is lightly sedated at this point, but continues trying to get out of bed. The drip is increased to 30 mcg/kg/min and the patient achieves light sleep. He is asleep soundly and snoring but responds to verbal stimuli. Saturations remain at 98% without supplementary oxygen. He is admitted to the MICU.



1. Which of these is indicated in treatment of acute benzodiazepine overdose?

A. activated charcoal

B. gastric lavage

C. flumazenil

D. naloxone

E. supportive care


2. What are sequelae of benzodiazepine withdrawals?

A. agitation

B. seizures

C. hallucinations

D. nausea

E. all of the above


3. Which BZDA has a risk of propylene glycol poisoning when given IV for prolonged periods?

A. ativan/lorazepam

B. versed/midazolam

C. xanax/alprazolam

D. klonopin/clonazepam

E. onfi/clobazam



4. What is the approximate LD50 of Valium (diazepam)?

A. 1 mg/kg

B. 10 mg/kg

C. 100 mg/kg

D. 1000 mg/kg

E. unknown



1. E

2. E

3. A

4. E


GOAL: The benzodiazepines are a class of medications that are critical to the armamentarium of emergency medicine physicians. In order to never harm a patient, it is important to touch up on some important facts and continue to think critically about the medication and the patient every single time one places an order for a benzodiazepine. Learning the short-term and long-term effects as well as the limitations of medications allows physicians to be more confident when using these medications.

1. Which of these is indicated in treatment of benzodiazepine overdose?


We are taught in our didactic teachings and USMLE exams that Flumazenil is the antidote for benzodiazepine overdose. Yet, in the setting of the Emergency Department, there is relatively little utility to Flumazenil, for more than one reason. Primarily, Flumazenil has been known to lower seizure threshold in chronic Benzodiazepine users, and this is a risk that is just not worth taking when the patient rarely needs anything more than supportive care. Additionally, there is rarely a situation during which we can be fully confident that the patient we are treating has no other co-ingestions in addition to the benzodiazepines, and there are many documented cases in literature demonstrating seizures in patients with co-ingestions that receive Flumazenil.

There is no place for gastric lavage or activated charcoal in the treatment of benzodiazepine overdose. In fact, in treatment of benzodiazepine overdose without co-ingestion of another drug or alcohol, the patient is likely to benefit most from simple supportive therapy with IV fluids and airway protection. If the patient is not responding well, or requires a rapid return of mental status, such as in the case of accidental iatrogenic overdose, the patient may be treated with Flumazenil. Flumazenil may be given in boluses of 0.3 mg IV spaced at 5 minute intervals for a maximum of 3 mg/hr.

2. What are the sequelae of benzodiazepine withdrawals


Benzodiazepines themselves work at the GABA receptors of cell membranes, allowing for an increase in opening frequency of the chloride ion channel, which hyper polarizes the cell, therefore causing an increased potentiation of the GABA neurotransmitter’s overall inhibitory properties. Therefore, sudden lack of the drug after prolonged use causes a hyperactive state so to speak. The patient may become incredibly agitated or aggressive, even psychotic. Patients can have hallucinations, seizures, insomnia, muscle spasms, and delirium.

3. Which BZDA has a risk of propylene glycol poisoning when given IV for prolonged periods?


Propylene glycol is used as a diluent in the formulation of IV preparations of both Ativan (lorazepam) and Valium (diazepam) to help dissolve the drug into the solution. The prolonged IV administration of either of these two drugs causes an increase in the concentrations of propylene glycol, which causes a constellation of symptoms of toxicity much like that of ethylene glycol. These begin with CNS depression, seizures, coma, and GI irritation. This can follow with tachypnea, pulmonary edema, tachycardia, hypertension, pneumonitis, or shock. Finally, the toxicity affects the kidneys, causing flank pain, hematuria, oliguria, or proteinuria. This can be fatal, and therefore avoiding the use of these two medications in prolonged IV administration is recommended.

4. What is the approximate LD50 of Valium (diazepam)?


It is true that this is truly unknown. Mice have an LD50 of ~700 mg/kg whereas rats have nearly ~1200 mg/kg. The important point is that Valium has an incredibly high therapeutic index of 1000:1, meaning the lethal dose is 1000 times higher than the effective dose. This is a comforting fact when administering such large doses as was given above. As patients are supportively monitored, there is often times recovery without permanent symptoms from acute intoxication. There are cases of acute ingestion of 2000 mg and 500 mg of diazepam with suicidal intent documented in case studies in 1978. The patients both fell into moderately deep comas but awoke with just supportive care and were discharged from the hospital within 48 hours of admission.


Rapid Recovery From Massive Diazepam Overdose. David J. Greenblatt, MD; Elaine Woo, MD; Marcia Divoll Allen, RN; Paul J. Orsulak, PhD; Richard I. Shader, MD. JAMA. 1978;240(17):1872-1874.

Fatal seizures after flumazenil administration in a patient with mixed overdose. Haverkos, DiSalvo, Imhoff. Ann Pharmacother. 1994 Dec;28(12):1347-9.

Senior Report 8.15


Case Presentation by Brian Holowecky, MD

CHIEF COMPLAINT  “I have a sore throat and I cannot breathe”

54-year-old female presents to the emergency department brought by ambulance for sore throat. She states she has had a sore throat since this morning and it has been getting progressively worse. Her throat feels like it is “closing up.” She called the ambulance because she was having increasing difficulty catching her breath. She feels a swelling in her throat which is causing her to be unable to drink or eat anything. She has a history of allergy to lisinopril. She has had angioedema reactions.  She admits to using crack cocaine last night out of a pipe in which she has done many times in the past. No fevers. No upper respiratory symptoms recently. No recent coryza symptoms. On further questioning she states that but used a larger amount of cocaine than usual last night.

REVIEW OF SYSTEMS:  Negative except as in HPI

PAST MEDICAL/SURGICAL HISTORY  History of angioedema, Hypertension, diabetes, asthma, bipolar disorder,
MEDICATIONS:  Albuterol, fluticasone, fluoxetine, clonidine, amlodipine, loratadine, omeprazole.
ALLERGIES:  Lisinopril, anaphylactic.
SOCIAL HISTORY:  Tobacco use, recent crack cocaine use yesterday by a pipe inhalation, heroin abuse. Recently attempted inpatient rehabilitation for drug abuse.

Vitals: BP 166/93 heart rate 58 respirations 16 temp 37.0 saturation 100% on room air.
General: Well nourished patient appearing mildly toxic in respiratory distress. She is hoarse. There is some questionable stridor.

HEENT:  Posterior pharynx is mildly erythematous initially. Mucuous membranes moist. No cobblestoning. Uvula is midline. Mallampati score is 2. Lips are not swollen. No periorbital edema.

Cardiovascular:  S1 S2. RRR. No murmurs. Peripheral pulses equal bilaterally.

Respiratory: Hoarse voice. Stridor. Increased work of breathing. Sitting forward in sniffing position. Breath sounds are equal. No wheeze or crackles. Tolerating secretions initially.

Gastrointestinal:  Soft, NT ND. No rebound, guarding, or rigidity.

MSK/Extremities:  No gross deformities. No joint swelling, erythema. No edema.

Skin:  Warm and dry. No rashes, bruises, or abrasions.

Neurologic:  Alert and Oriented. Follows commands. No facial asymmetry noted. Motor and sensation intact.

Medical Course:  
Initially concerned for anaphylactic reaction in this patient with a known history of anaphylaxis. She was appearing very anxious and beginning not to tolerate her secretions very well. There was slight drooling. I was concerned based on her deterioration for anaphylactic reaction. She began to get more hoarse of voice and to sit forward in the sniffing position. There was questionable stridor.

She received 0.1 mg of epinephrine IM, along with Zantac, 125 mg of Solu-Medrol, 50 mg of IV Benadryl. She did improve somewhat at that time.

The working diagnosis was possible anaphylactic reaction versus anxiety or panic attack. This is a patient with a known psychiatric disorder. She was placed on the cardiac monitors and continuous pulse ox. IV access was established. She began to tolerate her secretions better at that time. Her heart rate remained in the 50s to 60s. Saturation remained 100% on room air.

About 90 minutes into her ER visit, she appears to be worsening and begins tripoding, drooling more profoundly and acting considerably more anxious.  Shas never had any visible airway swelling.

A lateral neck xray is taken:



1) What is the most likely cause for her condition?
A) Anaphylactic reaction from unknown source
B) Thermal pharyngeal Injury
C)Neoplastic transformation of a previously benign lesion
D)That is a normal lateral neck xray. There is no abnormality.

2) What is the treatment for her condition?
A) Urgent intubation in a controlled environment
B) Admission an ICU for close airway monitoring
C) Steroids, antihistamines, and H2 blockers.
D) Antibiotics and ENT consult for drainage.

3) If you suspect anaphylaxis, what is the appropriate initial treatment?
A) 0.3 mg epi subQ, 50mg diphenhydramine, 150 mg ranitidine, steroid
B) 0.3 mg epi IM, 50mg diphenhydramine, 150 mg ranitidine, steroid
C) 0.1 mg epi sub Q, 50mg diphenhydramine, 150 mg ranitidine, steroid
D) 0.1 mg epi IM, 50mg diphenhydramine, 150 mg ranitidine, steroid

Bonus Question 1: Should an epipen be administed into the thigh of the person with the suspected anaphylactic reaction, or into the thumb of the person holding the autoinjector?
A) Thigh
B) Thumb

Bonus Question 2:  Do vaccines cause autism?
A) Yes
B) No

1) B
2) A
3) B

Bonus Questions:
4) B

This patient ended up being found to have crack cocaine induced probable thermal epiglottitis.  It presented atypically, which is how epiglottitis tends to present in adults.  Epiglottitis is a rare finding in the post vaccination world.  Thermal injury is known to cause edema and epiglottitis.  Embers from a pipe or bong may be inhaled and cause thermal burns to epiglottis. In this case no thermal burn was visualized, but patient had clear epiglottitis presumably from cocaine. Imminent airway compromise is possible, if not suspected and treated appropriately.  Crack cocaine is known to cause “crack lung” but crack cocaine epiglottitis has only been reported once before in the early 1990s.

When suspicious for epiglottitis the appropriate course of action is to proceed with intubation with extreme caution.  Laryngeal and epiglottic spasm is very common.  Intubation in the OR with preparation for a surgical airway is desirable.  The diagnosis can be made with lateral neck xray as it was in this case, however another way is by direct visualization with fiberoptic ENT scoping.

Anaphylactic reaction was on the differential and the patient received treatment for anaphylactic reaction, albeit somewhat incorrectly.  Subcutaneous epinephrine has been shown to be less efficacious than intramuscular administration.  In cases of anaphylaxis, the subcutaneous vasculature is constricted and so dissemination of the epinephrine systemically is delayed as compared with intramuscular direct administration.  Remembering dosing and administration is critically important in timely management of anaphylaxis, and epiglottitis too.