Intern Report 8.26



Case Presented by Barry Kang, MD


Patient is brought into resuscitation as a trauma code 1. He has been shot multiple times in the chest. He is intubated and is swept off to the operating room. As your are leaving the resuscitation bay a DPD officer approaches you and asks you about the patient and what is going on. What do you respond?

a) I’m sorry sir the only thing I can tell you is that the patient is in critical condition and that he is one his way to the operating room.
b) His name is John Brooks and he got shot multiple times in the chest and abdomen. He had to be intubated and is in critical condition. He was just taken to the operating room.
c) He is middle age African American male who has sustained multiple gunshot wounds and was just taken to the operating room.
d) Here is FIN number with his name, age and birthday. He has sustained multiple gunshot wounds to the chest and abdomen. He was just taken to the operating room.


2) You have just seen an interesting case in MOD 2 and the patient was just sent up to the MICU. The intern in MOD 2 has just started their shift at 9am. You think it’s a great case to learn from and want to tell the intern about the case. What should you do?

a) Give them a sticker and tell them to look up the labs, ECG, HPI and physical you just finished dictating. After that ask them what they think.
b) Give them the ECG and ask for their interpretation.
c) Present them the HPI and physical and show them the ECG without the top strip with the reading and patient information.
d) Don’t talk to them about the case because it would a HIPAA violation.


3) You come in for a shift and check your mail box in 3R, you have received a subpoena from a law firm requesting the medical records and your testimony about a patient you had seen about 6 months previously. It turns out the patient is suing his employer since he was hurt at a job site and received care from you after the accident. What should you do next?

a) Ignore it. Someone else will deal with the legal aspect, you didn’t get into medicine to deal with legal system.
b) Send all the medical records to the law firm. It’s ok since they are representing the patient.
c) Contact the patient and ask them to fill out a medical release form.
d) File the form away and take care of it when you have more time.


Bonus Question: You walk into MOD 6 to evaluate a patient for altered mental status. You see an 85 year old male who looks thin. He has stool caked onto his backside and after you clean this off you see multiple decubitus ulcers along his backside. Over the course of his ED evaluation his mental status has improved and you begin to talk him about what happened. He states that he lives at home with his son. He says sometimes his son doesn’t come and check on him all day. He is unable to ambulate on his own and has to sit in a dirty adult diaper. What is your role in this situation?

a) Tell the patient he can file a report of abuse if he wants.
b) Tell him that you are sorry for his living conditions and tell him a geriatric consult has been put in for further evaluation.
c) Report elder abuse and admit the patient for placement in a nursing home since he is not getting the care he needs at home.
d) Ignore the situation and move on to the next patient.


Answers & Discussion
1) Answer B – According to Michigan State law MCL 750.411 a physician or surgeon who is caring for a person suffering from a wound or other injury inflicted by means of a knife, gun, pistol, or other deadly weapon or means of violence, has a duty to report that fact immediately by telephone and in writing to the chief of police or head of the police force in that area they are practicing in. The report shall state the name and residence of the person if known, along with his or her whereabouts, the cause, character, and extent of the injuries and may state the identification of the perpetrator if it is known. So in this case the best answer would be B given the fact that you know the patient’s name and other pertinent information about the gun shot wounds. Answer D has more information than mandated by law and given the fact that HIPAA states that you are only allowed to give information if the patient is a victim of a crime, unless mandated by state law this may be too much information in the eyes of HIPAA.

2) Answer B – HIPAA states that you are only allowed to share protected health information for treatment, payment or healthcare operations. Treatment is defined as the provision, coordination, or management of healthcare or related services for an individual by one or more healthcare providers. Basically this states that information may be exchanged between anyone directly involved in the patient’s care or for any referral of care between providers. If the intern is not going to be involved in the patient’s care then they should not be in the patients medical record or other sensitive patient identifiers or information.

3) Answer C – Michigan state law states that the only time you are allowed to release protected health information in a legal arena is with a court order, which is a written order by a judicial officer or court of law. A subpoena may be issued from a lawyer and this may be for records or for an appearance in court. The only other time a physician is able to release protected health information without the patient’s consent is when the patient files or notifies the physician they intend to file a malpractice lawsuit MCLA 600.2157. Preferably you can refer the law office to medical records after the law office obtains the patient’s written consent.

Bonus) Answer C – MCL 400.11a states the healthcare providers are mandatory reporters for elder abuse. This report must include, under Michigan State law, name of the abused, description of the abuse, neglect or exploitation, the abused age, the name and address of the abused guardian or next of kin, and any information that might help determine why the abuse/neglect is occurring. Michigan statue voids the physician-patient relationship privilege in these situations.


Key Points

  • When working in the ED you do not have the right to open up and look at anyone’s chart You must have a doctor patient relationship, in other words you are directly caring for the patient
    look over and review the states laws in the area you are practicing state laws will give more specific instruction while HIPAA provides a more overarching guideline
  • When dealing with HIPAA specifically you’ll never be faulted for withholding/protecting a patients medical information
  • In the end similar to medicine in general if you do what is best for the patient you will have at least at start of a defense if your decision is ever questioned.



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.

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.

Intern Report 8.12


Case Presentation by Jacob Jensen, MD

Chief complaint: nausea and vomiting

HPI: Patient is a 28 year old female with past medical history of developmental delay, schizophrenia, and hypothyroidism transferred to the ED from a skilled nursing facility for nausea and vomiting. Patient is not responding to questions, she is not accompanied by family or nursing home staff, and EMS is unable to supply further details. Per EMR review, patient is often transferred to this or other nearby hospitals with similar complaints (especially the day before holiday weekends).

ROS: Could not be obtained 2/2 patient’s underlying medical presentation.

PMH: Developmental delay, schizophrenia, hypothyroidism

PSH: There is a reference to an X-lap in the EMR but no explanation as to when or why it was performed.

SHx: Patient has resided in a skilled nursing facility for at least the last 10 years


Meds: seroquel, trazadone, respiredone, cogentin, synthroid,

Physical exam:
Vitals: T 36.4 Oral, HR 137, BP 49/33, RR 22, SpO2 97% on room air
General: Alert but non-verbal
Eye: Extraocular movements are intact
HENT: Normocephalic, Atraumatic, Oral mucosa is dry
Respiratory: Respirations are non-labored
Cardiovascular: Normal S1, S2, no murmurs, rubs, or gallops
Gastrointestinal: Soft, mildly distended, no rebound or guarding
Musculoskeletal: No deformity
Integumentary: Cool, dry, intact

Course in the ED:
Patient was triaged to resuscitation bay due to hypotension with tachycardia. A 16 gauge IV was started and patient was given 2L normal saline. On repeat testing, patients HR had decreased to 118 and BP had increased to 92/70.

Patient had one witnessed episode of vomiting in the ED. The vomitus smelled feculent so an NGT was placed. 300mL of yellow-green gastric contents was returned.

Basic labs were as follows; Bedside Glucose unremarkable, Lactic Acid 9.7, BMP unremarkable, CBC remarkable for leukocytosis of 13.1 with absolute neutrophil count of 9.7, coags unremarkable, urinalysis unremarkable, and urine pregnancy negative.

Chest X-ray was unremarkable.

EKG was unremarkable.

Abdominal series was obtained and read as suggestive of high-grade distal small bowel obstruction.



The patient is transferred to the module and a surgery consult is placed. On reexamination, HR is 115, BP is 120/68. The patient is now nodding and shaking her head in response to questions. When asked if she has any pain, she indicates her abdomen. Her abdomen is still mildly distended and diffusely TTP without guarding or rebound.

A) What is the most likely cause of lactic acidosis in this patient?

  1. Increased pyruvate production
  2. Reduced entry of pyruvate into mitochondria
  3. Accumulation of NADH
  4. Impaired gluconeogenesis
  5. Metabolization of glucose by intestinal bacteria

B) What is the best fluid replacement option in this situation?

  1. Crystalloid (Normal Saline or Lactated Ringer)
  2. Buffer therapy (0.45% saline solution with 75mmol/L of sodium bicarbonate)
  3. Blood products
  4. Albumin
  5. Hyperoncotic starch

C) What further diagnostic studies, if any, are called for?

  1. No further studies are necessary
  2. Check patient’s D Dimer
  3. Check patient’s liver function; AST, ALT, Alk. phos.
  4. Abdominal CT angiogram
  5. Exploratory laparotomy

Answers & Discussion
1) 3
2) 2
3) 6

A) What is the most likely cause of lactic acidosis in this patient?

  1. Increased pyruvate production
  2. Reduced entry of pyruvate into mitochondria
  3. Accumulation of NADH
  4. Impaired gluconeogenesis
  5. Metabolization of glucose by intestinal bacteria

B) What is the best fluid replacement option in this situation?

  1. Crystalloid (Normal Saline or Lactated Ringer)
  2. Buffer therapy (0.45% saline solution with 75mmol/L of sodium bicarbonate)
  3. Blood products
  4. Albumin
  5. Hyperoncotic starch

C) What further diagnostic studies, if any, are called for?

  1. No further studies are necessary
  2. Check patient’s D Dimer
  3. Check patient’s liver function; AST, ALT, Alk. phos.
  4. Abdominal CT angiogram
  5. Exploratory laparotomy


  1. First a quick recap of lactate production in human cells. In glycolysis, glucose is broken down into two pyruvate molecules. This pathway produces a total of 2 ATP, and also converts two molecules of NAD+ into two molecules of NADH. In aerobic environments, the two molecules of pyruvate can then be transported into the mitochondria to participate in the citric acid cycle producing more NADH. Finally, NADH is converted back to NAD+ in the electron transport chain of the mitochondrial matrix, creating a proton gradient that is used to produce more ATP. However, the electron transport chain can not operate in an oxygen poor environment. This means that without oxygen, the cell can not convert NADH back to NAD+. The solution to this problem is anaerobic glycolysis, during which pyruvate is converted into lactate, a process which regenerates NAD+.






Lactate, or lactic acid, can then be further oxidized into water and carbon dioxide or used by hepatocytes as the substrate for gluconeogenesis in the liver. Of note, human cells produce the L isomer of Lactic acid while bacteria can also produce the D-isomer which is not readily metabolized by human cells and can accumulate.

This patient presented in hypovolemic shock. It is not known how long she had been in this state, but it can be assumed that she has experienced some amount of end organ hypoperfusion. Insufficient oxygen delivery will result in the inability of mitochondria to maintain the activity of the electron transfer chain, resulting in a buildup of NADH. By Le Chatelier’s principle, an accumulation of NADH will drive the Pyruvate/lactate equilibrium toward the production of more lactate. This is what is causing our patient’s lactic acidosis.

Accumulation of NADH might also be secondary to increased metabolic demands such as during a grand mal seizure or intense exercise. However, this does not appear to be the case with this patient.

Increased pyruvate production (a) occurs in patients who have enzymatic defects affecting glycogenolysis or gluconeogenesis. This would most likely present in patients younger than 28 years old. Mitochondrial dysfunction (b) might also be secondary to genetic defects or it could be 2/2 drugs that cause mitochondrial damage. Examples of such drugs include Antiretrovirals and some antibiotics such as linezolid. There is no indication that this patient is taking any such medication.

Gluconeogenesis (d) mostly occurs in the liver. Patients with impaired liver function may have elevated lactic acid levels. Because this patient had an unremarkable coag profile, it is not likely that her liver is the source of her lactic acidosis.

D-Lactic acidosis (e) can be seen when intestinal bacteria are exposed to high levels of glucose. An example of this is patients with short gut syndrome. There is no indication that this patient would have increased levels of D-Lactic acid.


  1. Crystalloids (a) are as effective as colloids at expanding plasma volume and saline has the advantage of being less expensive.

It has been thought that adding sodium bicarbonate to half normal saline (b) might help to buffer lactic acidosis while decreasing the chances of developing hyperchloremic acidosis, but this is controversial. At a minimum, patient’s serum pH and bicarbonate levels should be tested before beginning this therapy.

Blood replacement therapy (c) is indicated if patient is actively bleeding, or has a low hemoglobin and is symptomatic, none of which apply to this patient.

No advantage has been found for albumin (d) in hypovolemic resuscitation and hyperoncotic starch (e) is not advised over concern for kidney injury.


  1. After resuscitation from hypovolemic shock, this patient was found to have elevated lactic acid, leukocytosis, and small bowel obstruction. She is non-verbal, but she does indicate that she is experiencing abdominal pain even though her abdomen is soft and there are no peritoneal signs. In this instance, the physician should have a low index of suspicion for mesenteric ischemia. The “gold standard” to evaluate for mesenteric ischemia is a mesenteric angiogram, however, recent studies have shown that CT angiogram has a sensitivity of 96% and a specificity of 94%.



Abdominal pain, lactic acidosis, and leukocytosis are all very non-specific. It may be very tempting to attribute these abnormalities to the small bowel obstruction and treat for constipation (a). However, mesenteric ischemia has not yet been ruled out.

D Dimer (b) is also a very non-specific test and would have little impact on the management of this patient.

This patient’s coag profile is within normal limits. She is not jaundiced, and there is nothing in her social history to suggest liver failure. Liver function test (c) would not influence the outcome of this case.

Exploratory laparotomy (e) is necessary if the patient has signs of intestinal infarction or perforation. As patient is hemodynamically stable and is not exhibiting peritoneal signs, Ct is more appropriate at this time.




  1. “Biphasic CT with Mesenteric CT Angiography in the Evaluation of Acute Mesenteric Ischemia: Initial Experience”, Radiology, October 2003. Kirkpatric et. al.
  2. “Fluid resuscitation with colloid or crystalloid solutions in critically ill patients: a systematic review of randomised trials”, British Medical Journal, March 1998, Schierhout
  3. Rosen’s Emergency Medicine, eighth edition, 2014, pages 1221-1224, Marx
  4. Uptodate, Causes of Lactic Acidosis, 2014 Emmett,
  5. Uptodate, Overview of Intestinal Ischemia in Adults, 2014 Grubiel and Lamont
  6. Uptodate, Treatment of Severe Hypovolemia or Hypovolemic Shock in Adults, 2014, Mandel and Palevsky

Intern Report 8.10


Case Presentation by Amy Buth, MD

A 12 y/o G0P0 presents to the ED with her mother and grandfather with complaints of vaginal bleeding for the past 20 days. Four days prior, she developed a severe frontal headache with fatigue. This morning she felt nauseated and had one episode of nonbloody/nonbilious emesis. She also developed diffuse abdominal cramps with extreme fatigue, leading to her collapsing at home. Her mother therefore brought her daughter in to the ED right away. Per the mother, the patient has irregular heavy periods which last 7 -10 days. Menarche was December 2013. Last cycle was October 14-November 4, 2014. She missed her cycle in August and September of 2014. During the past 20 days, she has been using 10 pads/day and noticing clots. She is not sexually active and denies any trauma or abuse. She currently feels weak and dizzy. She denies any fevers, chills, chest pain, shortness of breath, dysuria, hematuria, increased urgency or frequency with urination, or diarrhea.

PMH: Asthma (resolved)
SurgH: Right inguinal hernia repair 2011
Gyn: G0P0. Began menstruating December 2013; typically as a 7 day cycle
Meds: Tylenol for pain PRN
Allergies: none
FH: Denies family history of bleeding, bruising, thrombotic disease, breast/uterine/ovarian/colon cancer, hypertension, or diabetes
SH: denies alcohol, tobacco, illicit drug use. The patient is a Jehovah Witness


Vitals: Temp 37.0 oral, BP 120/66, HR 118, RR 20, 98% on RA. Positive orthostatics

Constitutional: Lethargic, poor eye contact, laying on the bed in mild distress.

Eye: PERRL, EOMI, no discharge, conjunctival pallor

Respiratory: Lungs CTA bilaterally, no cough, no wheezing, no cyanosis.

Cardiovascular: Tachycardia, regular rhythm, no chest pain, no palpitations, no peripheral edema, good pulses equal in all extremities

Gastrointestinal: Bilateral lower quadrant tenderness, no distension, no rebound tenderness, no palpable masses

Genitourinary: Pelvic exam: normal external genitalia, blood at the introitus, blood noted in the vaginal vault, there is slow active bleeding from the cervix. Bimanual exam: uterus is anteverted and normal in size, no adnexal masses or tenderness, no cervical motion tenderness

Integumentary: Warm, dry, pallor

Hematology/Lymphatics: No petechia or bruising

Neurologic: Symmetric face, decreased strength in all extremities bilaterally secondary to fatigue and poor effort


Pregnancy test: negative

CBC: 6.8>4.6/14.7<393 with 77% PMNs and 19% lymphs. MCV 75 and RDW 13.6

BMP: 137/3.8/103/24/11/0.52, glucose 98

Lactate 2.8

PT/PTT/INR: 11.4/21.5/1.07

TSH 6.149 (NL 0.210 – 4.940), T3 total 139 (NL 60 – 180), T3 free 3.9 (NL 1.4 – 4.4), total Thyroxine 8.7 (NL 6.2 – 14.6), free Thyroxine 1.1 (NL 0.8 – 1.8)

Prolactin 15.3 (NL 2.8 – 29.2)

von Willebrand activity 348 (NL 43-138), von Willebrand antigen 244 (60-153), Factor VIII 395.7 (63-150)


1) What is the patient’s most likely diagnosis?
a) Leiomyoma
b) Hypothyroidism
c) Anovulatory bleeding
d) von Willebrand Disease

2) After placing the patient on a cardiac monitor and starting a fluid bolus, what would be the best next step?
a) Uterine packing
b) Order O negative blood
c) Order a stat transvaginal ultrasound
d) Consult pediatric gynecology

3) What is the typical treatment for this diagnosis?
a) Gonadotropin-releasing hormone agonists
b) Synthetic thyroid hormone therapy
c) High dose estrogen therapy
d) Desmopressin / DDAVP

4) BONUS: The patient and her family are Jehova’s Witnesses. You develop great rapport with the family and have a heart to heart discussion about the patient’s treatment and safety. The patient and her family are grateful for your recommendations but are refusing a blood transfusion. They are agreeable to discuss alternative treatment plans. The patient is tachycardic, lethargic, orthostatic, and actively bleeding with Hg 4.7. You again strongly encourage the importance of the blood transfusion. The family then asks to be discharged so they can go to another Children’s Hospital that has a Jehovah’s witness liaison for more direction. What do you do?
a) Follow the patient/family’s wishes and do not give a blood transfusion. Consider other options.
b) Discharge the patient so they can go to another facility of their choice
c) Contact the court to make a ruling
d) Call security to keep the patient and proceed to give the blood transfusion

1. C
2. B
3. C
4. D



Question 1: Perimenarchal adolescents who have abnormal uterine bleeding typically results from anovulation (C). During the anovulatory cycle, estrogen levels rise but in the absence of ovulation, a corpus luteum never forms. Therefore, progesterone is not produced, causing the endometrium to become hyperproliferative. Once the endometrium outgrows its estrogen supply, it leads to irregular sloughing and bleeding. Sometimes anovulation occurs from an abnormality in the hypothalamic-pituitary-ovarian axis. The hypothalamus secretes GnRH which stimulates the pituitary to produce FSH and LH which act on the ovarian follicles and ovarian theca cells respectively. If there is an alteration to the GnRH release, this will affect FSH and LH. Thus, if there is a decrease in GnRH such as with hypothyroidism (C), this leads to decreased FSH/LH that may result in amenorrhea. Increased prolactin can also lead to GnRH suppression and amenorrhea. Hyperthyroidism on the other hand would lead to menorrhagia. In this case, the patient had an elevated TSH but normal T3/T4 results which suggests subclinical hypothyroidism which would not cause the irregular heavy bleeding. She also had a normal prolactin level. Polyps, leiomyomas (A), and ovarian neoplasms leading to irregular bleeding are less frequent in this young adolescent group. If there is considerable bleeding around menarche enough to necessitate blood transfusions, coagulopathies like von Willebrand Disease (D) should be excluded. VWD is a common coagulation abnormality that arises from a deficiency of von Willebrand factor, a protein required for platelet adhesion, platelet-endothelial adhesion, and fibrin clot formation by acting as a carrier protein for factor VIII. In this patient, the von Willebrand activity (also known as the Ristocetin Cofactor) is elevated to 348 (normal 43-138), von Willebrand antigen is elevated at 244 (normal 60-153), and factor VIII is 395.7 (normal 63-150). Patients with VWD typically have normal to decreased levels of VWF antigen, VWF activity, and Factor VIII. A possible explanation for the elevated levels is that VWF is an acute phase reactant that could be elevated secondary to the patient’s clinical state.

Question 2: After running through ABCs and beginning fluid resuscitation, the patient should receive a blood transfusion (B) due to her Hg being 4.6 with tachycardia, lethargy, lightheadedness, fatigue, and positive orthostatics. This patient is symptomatic from her anemia secondary to vaginal bleeding. She is actively bleeding but not profusely bleeding due to a ruptured major vessel. Uterine packing (A) may be necessary in severe life-threatening blood loss. Specifically, a foley catheter can be placed in the cervix to tamponade the bleeding. Packing in light bleeding has increased risk of infection and is usually avoided. A transvaginal ultrasound (C) is needed, but should wait until the patient is stable for imaging. Pediatric gynecology (D) should be consulted but the patient is unstable and needs blood products first.

Question 3: The treatment for anovulatory bleeding in this patient is high dose estrogen therapy which should be initiated after OBGYN consultation and recommendations (C). If Hg >12 g/dL you can supplement with iron, NSAIDS to help reduce flow, and consider oral contraceptive pills if the patient is sexually active. If Hg 9-12 g/dL, OCP BID until bleeding stops and continue OCP QD for 21 days followed by 1 week of placebo pills. If Hg <9 g/dL, admit to hospital and transfuse based on degree of hemodynamic instability. OCP Q4H until bleeding slows and then OCP QID for 2-4 days followed by OCP TID for 3 days, and then OCP BID for total of 21 days or until HCT >30%. Gonadotropin-releasing hormone agonists (A) can be used for temporarily shrinking uterine fibroids and temporarily stop menstrual bleeding. Hormonal birth control can also be used to reduce bleeding, cramps, and pain for women with fibroids. Synthetic thyroid hormone therapy (B) is used for hypothyroidism. Desmopressin / DDAVP (D) is used for von Willebrand Disease. It is known to increase VWF and factor VIII levels.

Question 4: This is a tricky ethical question because the patient herself is refusing blood as well as her parents. She is a minor and cannot make decisions on her own at this point. In general, if a child needs blood to save his/her life, you must give blood (D) – even over the objection of the patient and parents. Parents do not have the right to refuse life saving treatment for a minor. It is important though to seek parental consent for their child even if they refuse. This may lead to a constructive conversation that could provide the family with a better understanding of why the patient needs the blood transfusion. In this particular case, the blood products were ordered, and the ED physicians and the family had a long conversation about the benefits and risks of the transfusion. The family kept refusing the transfusion. Hematology was consulted to see if there was any other option to treat the anemia. They said blood was necessary. Therefore, two services and two ED physicians were in agreement to the blood transfusion. By this time, the blood arrived, and the family tried to leave AMA. The ED physicians called a member of the ethics committee who agreed the patient’s safety takes over and a blood transfusion was necessary. Fortunately, good rapport was eventually made between the family and the physicians, and the family finally signed consent for a unit of packed red blood cells. OBGYN was involved and initiated Premarin.


Hoffman BL et al. Chapter 8. Abnormal Uterine Bleeding. Williams Gynecology, 2eNew York, NY: McGraw-Hill; 2012.

Morrison LJ, Spence JM. Chapter 99. Vaginal Bleeding in the Nonpregnant Patient.  Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 7e.New York, NY: McGraw-Hill; 2011.

Rick, Margaret. Treatment of von Willebrand disease. UptoDate. Nov 1, 2013

Sass AE, Kaplan DW. Adolescence.  CURRENT Diagnosis & Treatment: Pediatrics, 22eNew York, NY: McGraw-Hill; 2013.

Stewart, Elizabeth. Uterine Fibroids: Beyond the Basics. UpToDate. Oct 11, 2013

Image courtesy of ScienceBlogs: Pharyngula.