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Global Fever…

Being covered 24/7 by news networks is the latest health scare…swine flu. The World Health Organization (WHO) has declared it a phase 4 pandemic alert (confirmed person-to-person spread of a new influenza virus able to cause “community-level” outbreaks”).  As I watch the news to try and understand what is going on, I’m given images of people in masks, especially in Mexico City, travelswine-flu-outbreak-in-mex-001 alerts for those planning traveling in and out of the United States, and a clean bill of health for President Obama after his recent travel to Mexico and overseas. But lost in all of this is actual information is relevant information of what the swine flu is, how it came to be, what to look for, and why are we freaking out about it.

The swine influenza virus is a virus found to be endemic amongst pigs. There are 2 of the 3 viruses that are responsible for swine flu can also affect humans. Those who work with poultry and pigs are at risk of infection if the animals carry the virus that can infect humans. However, the virus is usually not passed from human to human, unless a mutation has taken place. This is the theory behind the current outbreaks that have taken place. Epidemiologists believe that the initial spread may have occurred at a swine farm outside of Mexico City. Spread of the disease has occurred as people have traveled into Mexico City affecting locals and travelers, who then travel out of Mexico and to other countries.

Mexico Swine FluSymptoms are very similar to that of the common influenza virus that we are familiar with…fever, fatigue, coughing, sneezing, lack of appetite, vomiting, diarrhea, generalized body aches. As with most viruses, it is spread through casual contact and well as respiratory droplets (coughing, sneezing). Usual hygeine practices (such as frequent hand washing with soap and water!) can greatly reduce the spread of any influenza virus. There have been no reported cases of transmission of the virus within pork products.

Treatment that is currently recommended include using Tamiflu (oseltamivir) or Relenza (zanamivir), as resistance has been seen with amantidine and rimantidine. This bears the question of who should be treated. Currently it is recommended that those with recent travel areas to Mexico or exposure to reported cases and influenza symptomatology should undergo nasal swab testing. If the nasal swab is positive for influenza A and have severe symptoms, including multiple comorbities, these patients should be admitted with respiratory droplet precautions, and started on olseltamivir. Those with less severe symptoms can be treated as an outpatient and provided with a respiratory mask. Those that test positive for Influenza B should be given supportive treatment for influenza. High index of suspicion is key….make sure you obtain a good history including start of symptoms and exposure risks.

Why is this flu so concerning? Reportedly, there have been deaths in otherwise young, healthy individuals that would otherwise not get so sick from an influenza virus. In addition, cases reported from 5 states in the United States, as well as Scotland, Spain, Canada, New Zealand, and Israel are creating concern for quick global spread.04-27-2009n1a_27flugul2k4kf31

Working in a busy emergency room, it is expected that we are going to have many patients concerned about the swine flu and seeking treatment for their symptoms. Patient education will be key, as many will flu-like symptoms, but will most likely not have the swine flu. The best thing you can do is educate yourself, educate your patients, and take into consideration symptomatology, risk factors and exposures, and patient comorbidities.

Here’s a global photo gallery courtesy of National Public Radio

For more information:
Centers for Disease Control
World Health Organization

Dr. Marjan Siadat is a second-year Emergency Medicine resident at Detroit Receiving Hospital, Wayne State University. She is the editor of the public health section for Receiving.

Intern Report Case 1.9

intern-report

Presented by Mondeep Narewal, MD

HPI:
A 55-year-old man presents to the ED for progressive shortness of breath. His past medical history is significant for congestive heart failure, chronic obstructive pulmonary disease, diabetes hypothyroidism, and kidney failure.   Only a limited history could be obtained as the patient is short of breath.  He states that he has been getting short of breath for the past week.  He also states that he has had some increased swelling in his feet and hands.  He usually is on  home oxygen  however has noted he needs more now.
Pt states he has had a cough and sputum production but no changes from baseline.
He has three pillow orthopnea and PND.  Patient states he has been compliant with all medications.

A review of his medical record shows that the patient was admitted 2 weeks prior for progressive shortness of breath secondary to CHF and it is noted that he has a dilated cardiomyopathy.  His ecocardiogram during this admission revealed an ejection fraction of 45%.

ROS: (limited secondary to shortness of breath)

He states he is fatigue and feels cold over his body.  Denies any chest pain, diaphrosis, palpitations.  No vomiting, no dizziness.  He states that he has been slightly more constipated than usual.  No blood per rectum.  No diarrhea.

PMH:
CHF, COPD, DM, hypothyroidism and chronic renal insufficiency

Medications:
Carvedilol, levothyroxine, , insulin, albuterol, sprivia, ASA

Allergies:NKDA

Social:
Positive for smoking history, no crack or cocaine or drug use.  Denies any ETOH.

Physical Exam:

VS:  T=35.1 Oral, HR=67, RR=28 BP=138/94 O2 Sat=87% on 2 L
General:  Pt  has a significant conversational dyspnea and appears in mild to moderate respiratory distress
Face:  Symmetrical simile no focal deficits has some non-pitting edema around the eyes.
Eyes: Conjunctiva pale, PERRLA, EOMI,
Ears: Clear TM
Mouth:  Slightly enlarged tongue no erythema no exudates.
Neck: Supple, enlarged thyroid gland that is non tender, no bruits heard, there is a JVD 7cm, trachea midline
Cardiac:  normal S1 and S2, has an S3,no murmurs, no rubs, regular rhythm
Lungs: Rales at both bases, wheezing diffusely throughout both lung fields.
Abd: Obese, soft, NTND, no rebound no guarding.
Extremities: Pulses symmetrical 2+ throughout, 2+ edema pitting in lower legs.
Neuro Exam:  Patient has no focal deficits, CN II-X12 (8 not tested) grossly intact.
Patient’s strength is 5/5 moving all extremities, has decreased reflexes at both patella and biceps but symmetrically decreased no clonus.
Skin Exam:  Dry cool skin, patient feels cool to the touch, cap refill is slightly prolonged, there is no erythema or lesions.

Lab Results:
CBC:  H/H 13/39, WBC: 12, Plt 190
Lytes:  132/4.4/107/26/2.5  Glucose=140
UA:  Negative
Troponin <0.02
Mg 2.1
TSH:  50 uIU/ml

EKG: NSR, Slightly flattened T waves, no ST depression or elevation,  prolonged QTc interval

CXR: Pulmonary congestion with b/l pleural effusions no cardiomegaly.

Questions:

1.  Taking the patient’s presenation into consideration, which of the following is the most likely diagnosis?
a)    Sepsis
b)    Congestive heart failure
c)    COPD exacerbation
d)    Hypothermia
e)    MI

2.  Given the patients clinical presentation and lab results what would be the most likely reason that this patients underlying condition has worsened?
a)    MI
b)    Uncontrolled Diabetes
c)    Pneumonia
d)    Noncomplaince with medications
e)    Thyroid function

3.  Given this patient’s clinical presentation, what is the most appropriate immediate management?

a)    Supplement O2, furosemide, nitroglycerin
b)    Supplement O2, steroids, albuterol atrovent
c)    Supplement O2, beta-blockers, furosemide
d)    Supplement O2, furosemide, nitroglycerin, start low dose levothyroxine
e)    Supplement O2, furosemide, nitroglycerin, start high dose IV levothyroxine replacement

Please submit your answers to the questions in the “leave a reply” box or click on the “comments” link.  Your submission will not immediately post.  Answers with a case discussion will post on Friday.  If you have any difficulty, please contact the site administrator at arosh@med.wayne.edu. Thank you for participating in Receiving’s: Intern Report.

#2: Turkey, Tinea, and a Touch of Death

sully-with-blood-drops2Sorry about the long silence. As you’ll see from this installment, I’ve been occupied. Hope this (long) post makes up for it. – Sullydog

The Rapid Care clinic hasn’t opened yet, and the acute care mods are beginning to feel like the protracted combat sequence at the end of Children of Men. Yet another patient pops up on my congested list: “scalp rash x 3 mo.”

Unbelievable, I think to myself. Who could possibly think that a scalp rash was an emergency? After 3 months? And what person not at death’s door would come to the ED on a beautiful spring day like this, the first warm day in what seems an eon?

My resident is tied up with a complex lac. That’s okay–on the face of it, this doesn’t look like a teaching case. When I enter the module, I am confronted by an obese, anxious lady with a rip-roaring case of tinea capitis that I diagnose from across the room.

I manage a smile that is marginal at best, and squelch my impatience with this silly lady by reminding myself that this case is likely to be quick. Diagnose, treat, street, and back to the “real” patients.

“Hi,” I say, and introduce myself. “I’m one of the emergency doctors.”

She looks me in the eye, and there’s a hint of terror in her expression. “Doctor, I just want to know if I’m okay. I don’t want no aneurysm or cancer.”

Huh? I’m closer now, and I’m 100% certain that this is tinea.

“Um…no,” I tell her, a bit bemused. “That’s not…cancer.” I immediately double-check myself and look again. I squint at it to see if I can make it look like cancer. Nope. That’s tinea.

“I had cancer,” she tells me. “I had cervical cancer.They almost didn’t catch it in time.”

Not only am I sure that this thing on her scalp isn’t cancer, I’m absolutely positive that it isn’t cervical cancer.

“No,” I tell her. “It’s just tinea.”

The unfamiliar word frightens her. Her eyes get wide. “What’s that?

“It’s a fungus. It’s just ringworm. We can clear it up.”

She starts to relax. “It’s not an aneurysm, either?” Her mother, as it turns out, had a an aneurysm, something in her head that killed her. She’s heard that they’re hereditary.

“No, that’s not an aneurysm, I’m sure.”

She grimaces and shakes her head. “I just want to know if I’m okay.”

“I have to ask,” I tell her. “If you were that worried about it, why didn’t you come in earlier?”

She looks at her feet and nods, a sort of silent mea culpa. “I know,” she says. “Stupid.”

Uneducated, I think, but not stupid. By now I’m starting to forget that this lady’s appearance in my ED is cramping my style, messin’ up my rhythm. She’s gone from being a treat-n-street to a person. It’s a humbling moment, of the kind that come–or should come–quite often in emergency practice. There’s no such thing as a good slow emergency doc, but sometimes we do need to slow down a bit just to remember why we’re here. I sit next to her. “No, it’s not stupid,” I say.

“I was just scared. I thought it was cancer. I mean, not really, but I thought it might be.”

I’m suddenly awake to what’s going on. This lady–not particularly knowledgeable, and with limited resources at her disposal–has been trying for three months to work up the time, energy and, most of all, the courage to come down here and just find out whether she’s okay…or if maybe she’s going to die.

Because, you see, she’s had brushes with death before. Unlike many of our younger patients, convinced of their own indestructibility, she’s got the age, the experience, the scars and the innate wisdom to know and fear her own mortality. She watched her mom die young of some mysterious thing called an aneurysm, which had something to do with her head, a genetic demon that might possess her as well. And she herself had to fend off a cancer that had come for her. Now she thought another monster was stalking her, and after three months of hiding from it she’s worked up the fortitude to come in and find out just how bad it is.

She just wanted to know that she was okay.

You and I are the same, I think, and at that moment she is the most important patient in the module.

Let me back up before any of you Bozos think I’m getting all soft and cuddly on you. Not likely. But about three months ago, I did have an interesting experience.

I started my shift at 1pm. It was the standard Mod 4 “afternoon overflow” shift. In all, my residents and I saw some thirty patients over the next ten hours. I had two very long codes during the shift, and most of our patients were complex, difficult, bizarre, drunk and demanding. It was a typical inner-city ED shift. I ate almost nothing, and drank far too much coffee.

At about 1130 pm, after my module had closed to new patients, I came to realize that I had not been taking very good care of a patient who had arrived many hours earlier. I was attempting to correct the deficiencies in my care and was having some difficulty getting the overworked nurses to recognize that he was sicker than I had thought. By midnight, my orders for additional fluids and repeat vital signs had not been carried out. My request to ICU that they admit him had also not been received favorably. All, ultimately, my fault; if I had made the relatively elementary recognition of his need for care hours earlier, I wouldn’t have been playing catch-up.

I stood at the bedside of my patient, painfully aware of the untimeliness and deficiency of my care–not an unusual circumstance for any emergency physician, certainly not for me. I was using my sergeant voice, imploring the staff to hop-to. I was upset with them, with ICU, and mostly with msyelf. And of course, I was exhausted, some 15 hours after rising, some 11 hours after starting shift. I suddenly felt flushed, which for an instant I attributed to my dissatisfaction with the situation and the dismay of letting my patient down. I have experienced this before, this sudden reddening and warming, the adrenal blush that accompanies stress in the ER. Flushing gave way to a sense of profound weakness and fatigue and a sort of vertigo. “I need to eat that sandwich I brought for lunch,” I thought. “I need to sit down and eat.”

Then I was in a dream, looking at a faraway TV screen displaying the faces of my colleagues arrayed in a circle. Then I was inside the screen, and I was in pain, and I fought back against them, and they were holding me to the floor. The Man With The Red Shoes, Dr. Phil, was shouting at me. It took some time to understand what he was saying, that I had passed out, fallen, and struck my head. Now he was flushed and upset, as were my other co-workers. I had really frightened them. Soon I was on a backboard and then on a gurney, with O’s in the nose and an IV and monitor leads on my chest. I was a patient in my own module.

The story became more clear as time went by and they filled me in. I had told one of my favorite nurses, in what she called a strange, sing-song voice, in a very automatic and rehearsed way, to do several things she had already done. “I need him on a monitor.” He was on a monitor. “I need him to get fluids.” He was receiving fluids by then. “We need to prioritize.” I remember saying none of this.

Then I went straight back, like a felled tree, and my head made a resounding crack that, allowing for some exaggeration from my excitable coworkers, was allegedly heard throughout our department. There was apparently some “Smurfication” of my complexion, and I had that empty, blinkless stare we don’t like to see in patients. The nurse could not find a pulse, probably because of profound bradycardia, and CPR was initiated. I woke up some thirty seconds into this code, physically combative, apparently with the words “Get the f**k up off me.” I do not recall that, either. I do recall that my head and neck hurt, and my first quasi-lucid thought was to confirm to myself that I could wiggle my toes, extend my thumbs, shrug my shoulders, exercise my ocular muscles in all planes, and squeeze my own butthole. This I did. A relatively sophisticated clinical self-evaluation, at a moment when I could not recall my own birthday or phone number when asked.

I was scared.

I needed to know if I was okay.

But my ED workup was negative, my colleagues and coworkers were wonderful, and an overnight in the CCU yielded little besides a bill. Cardiology told me to set up an appointment for a perfusion stress and an event monitor. I went home. (And no, contrary to all the rumors I’ve heard, I did not sign out AMA.)

Ultimately, I believe this was an incident of little practical consequence, though it was a tad embarrassing. But I am awe-struck at how how precipitously and inexorably my sensibilities were taken from me. One moment I was suddenly overwhelmed with fatigue and dizziness, with barely an instant to reflect upon a sandwich before consciousness left me. If it had been a lethal arrhythmia, my last worldly thoughts would have been of honey-roasted turkey and swiss cheese. I did not register what was about to happen to me, much less did I have time to marshall what would have been an ineffective defense, or even a clever parting quip. My last words would have been “We need to prioritize.” Better, I suppose, than “I know what I’m doing, dear,” or “I need my diaper changed,” but hardly worthy of a tombstone.

Just that quickly, death might have tapped me on the shoulder and taken me. Of course, I have been aware of this possibility for some time, but to experience this small taste of the Reaper’s power, so palpably and vividly, can really change one’s outlook.

Doctors tend to think of themselves as fighters against pain and disease and death. And I for one always fancied that I had a better personal chance against untimely death than the average Joe, simply by virtue of being an ED doc and in relatively good health. Of course I should have known better, and now I realize, as never before, that death need not face me like a combatant and grapple with me for my life. He can slip up behind me and cut my throat without a moment’s warning, whereupon I have barely enough time to register my own confusion before consciousness is gone. We are fighters, yes, but he is not. He will brook no opposition, and has no compunction about exercising his office without warning or trial.

My patient with tinea knows this better than I did just a short time ago, because she has had her own brushes with death. And she knows something else, too. She knows that death and disease are mysterious, even to doctors. Sure, she may not know how to tell tinea capitis from a skin cancer. But neither can my colleagues in the ED and in the cardiology clinic tell me why I zonked out in the middle of the module that night.

So even after my CT and my EKG and my serial trops and my other labs all came back 5/5, I, the big smart academic MD-PhD, was left with the same question that haunts my patient: Am I OK? Thereafter, every twinge of minor thoracic pain, every brief instant of fatigue or dizziness, every caffeine-induced palpitation made me wonder: Am I OK?

Two weeks after my episode, the resident who had been working with me that night approached me and asked me how my perfusion stress and event monitor had turned out.

“Well,” I said. “I…uh…”

Her eyes got wide. “No. You didn’t get them!”

“Well, now, look…”

“You didn’t follow up! I don’t believe it. You didn’t follow up!” She’s gaping at me.

Another resident overhears this. “What the f**k, dog?”

I am well-rebuked. Yes, I feel dumb. For two weeks I’ve been wondering: Am I okay? Do I have a renegade coronary? Some weird channelopathy that doesn’t show up on a cardiogram? Some insidious valvulopathy? Sick sinus? Epilepsy? Glioma? Oh, f**k–do I have brain cancer? Oh yeah. That’s it. It’s brain cancer. Or a valvulopathy. Or it’s a brain cancer and a valvulopathy. Do they go together? I bet they do. I bet there’s some weird syndrome of brain cancer, valvulopathy and syncope. A classic triad. Probably named after Quincke.

The only difference between me and my patient is that I can dream up far uglier and more ridiculous scenarios to explain my mysterious condition than than she can, by virtue of my training. But I’m apparently no more capable than she is of getting out from under the bed to do battle with these phantasms. It takes two weeks and a tongue-lashing from a couple of residents to get me to pick up the phone and make an appointment in cardiology clinic.

I put my hand on my patient’s shoulder. “It’s not cancer and it’s not an aneursym,” I tell her. “It’s just a fungus infection. It can be a little stubborn, but I can give you some medicine that should clear it up.”

She takes a deep breath and holds it. I can read her mind. She wants to hear the words.

“You’re okay.”

I can see the tension go out of her shoulders and her jaw muscles. She lets out a huge sigh and smiles. I’ve given her a reprieve from a sentence that we all must face eventually, a sentence that, in her mind’s eye, has hung over her head for weeks. I’m pretty sure I can help her tinea, but looking at her, I think that with two words I’ve already relieved more suffering in this one “non-teaching case” than I have all month. Something akin to the relief I felt when my cardiologist showed me the negative results of my perfusion stress, or when my three-week event monitor (what a pain in the ass!) came back negative. My world was exceptionally vivid after that clinic visit, my coffee quite bitter and delicious. I suspect my patient will find the fresh air outside today more pleasant than most of us would, the sunshine just that much more golden.

I shake my patient’s hand and go to write her prescription. You and I are the same, I think, feeling more like a doctor than I have all morning. But we’re okay.

Intern Report Case Discussion 1.8

intern-report

Presented by Rob Klever, MD

HPI
15 year-old female with a past medical history for asthma, who presents to the ED for a headache, myalagias and anorexia of two days duration.  She states that her headache is constant, located bilaterally frontal and of aching quality, relieved by laying down, worsened with movement and has intermittent photophobia. She reports last week that she a had a ‘stuffy nose’ and had one episode of diarrhea and vomiting.

Her grandmother states that took her to the pediatrician five days ago who diagnosed her with viral illness and gave her a prescription for amoxicillin that she took for two days then stopped because she had felt better before developing the headache.

ROS
Patient states that she as a mildly sore neck, but no stiffness.  Pt reports feeling malaised.

Patient denies any fevers, chills, nausea, vomiting, cough, congestion, wheezing, shortness of breath, chest pain, weakness, numbness or tingling in any of her extremities, constipation, diarrhea then the aforementioned week before, changes in bowel or bladder habits.

PMHx
Asthma, currently well controlled on no medications.
Medications: Albuterol prn
Allergies: NKDA

Social Hx
Patient states that several people in her church youth group have been sick lately, but denies any recent travel.
She lives at home with her grandmother and does well at school as a sophomore.
She denies any alcohol, tobacco and drug use.
She reports no sexual history and states last menstrual period was two weeks ago lasting normal duration and volume.

Family Hx
Positive for migraine headaches, negative for sickle cell and diabetes.

Physical Exam:
VS: Temp: 36.6C; HR 84; RR 24; BP 109/71; Wt 69.4 kilo
General: 15 year female who appears stated age.
Eyes: PERRLA, EOMI, sclera icteric, conjuctiva pale, fundoscopic exam shows sharp disc margins, no evidence of papillaedema.
Ears: TM clear
Tonsils: tonsils bilaterally 1+; no evidence of erythema, edema or exudates
Neck: soft, supple, no evidence of meningsmus.  No Kernig’s or Brudzinki’s sign present. Trachea midline.
Cardiac: RRR s1,s2; no m/r/g
Lungs: CTA B
Abdomen: soft, NTND, no evidence of HSM, no rebound, no guarding
Extremities: Patient moves all extremities spontaneously, normal muscle strength and tone.
Neuro exam: Patient has normal gait and station; patient has normal strength and reflexes in all 4 extremities.  CN II thru XII intact.
Skin: Warm, dry and well perfused.  Good skin turgor. No evidence of rashes, petechiae or bruises.  There is palmar pallor present.

Initial Lab Values:
CBC: WBC: 13.0; H/H 4.1/13.4; Plt 8
Na/K/Cl/CO2/BUN/Cr/Glu: 139/4.3/102/23/17/1.5/123
UA: Cloudy, Amber, SG 1.014, pH 5.5, 3+ Blood, 1+ protein, negative nitrite, trace leukocyte esterase, > 100 RBCs, 5-10 WBC, 2-5 RBC casts, 2+ bacteria
Urine β-HcG: Negative

Questions:

1)    Given the history and initial lab values, what is the most likely diagnosis?
a.    Urosepsis with associated DIC
b.    Idiopathic Thrombocytopenic Purpura
c.    Viral Meningitis caused by Parvovirus B19
d.    Catastrophic anti-phospholipid syndrome
e.    Thrombotic Thrombocytopenic Purpura

2)    What lab test do you want to order to confirm the diagnosis?
a.    Aerobic and Anaerobic Blood Cultures
b.    Hemoglobin Electrophoresis
c.    Lumbar Puncture
d.    Peripheral Smear
e.    PT/PTT/INR; D-dimer; Fibrinogen, Fibrinogen Split Products

3)    What is your initial ED management?
a.    Transfusion of pRBCs and Platelets
b.    High dose prednisone, pRBCs, FFP while awaiting Plasma Exchange Transfusion
c.    Early Goal Directed Therapy (Fluids, Antibiotics, pRBCs)
d.    Early intubation, Dialysis, Fluid Bolus, Platelets, Steroids, Broad-spectrum antibiotics
e.    Give methylprednisolone and IVIG

Discussion:

There is spectrum of TTP-HUS that involves a pentad of the following: microangiopathic hemolytic anemia (100%), thrombocytopenia (100%), renal insufficiency ((88%) with gross hematuria (15%)), fluctuating neurologic abnormalities AMS (36%) confusion, generalized headaches, altered mental status, focal deficits (12%), seizures (16%), visual disturbances, and coma, and fever (60%); with the understanding of that TTP has more neurologic findings and an adult disease with HUS has more renal and pediatric involvement.  It is a MEDICAL EMERGENCY and a CLINICAL DIAGNOSIS and you cannot wait for the other lab tests to come back before implementing treatment.  Without plasma exchange, mortality is greater than 90%.  Most cases of TTP arise from deficiency or inhibition of the enzyme ADAMTS13, which is responsible for cleaving large multimers of von Willebrand factor (vWF).  Treatment is aimed at reducing circulating antibodies against ADAMTS13 and to replenish blood levels of the enzyme via plasma exhange.  There are two exceptions to the general recommendation of plasma exchange in TTP-HUS: Post-diarrheal HUS in children and cancer chemotherapy or transplantation. Physical exam could show fever, hypertension, purpura, jaundice (ie, hemolysis), neurologic deficits (eg, altered mental status, seizure) and splenomegaly or be normal

In the emergency department after making the diagnosis you should begin looking for underlying causes such as pregnancy, cancers, medications including mitomycin C, cyclosporine, oral contraceptive, quinine, and ticlopidine.

Answers:

1)    E.  TTP
Given the fact that the patient has a hemolytic (scleral icterus) anemia (palmar and conjuctival pallor (Hgb 4.1), a severe thrombocytopenia (platelets of 8), acute renal insufficiency (Creatinine 1.5) and an neurologic abnormality (headache).  She meets 4/5 criteria for TTP-HUS.  This is an emergency and you would be amiss to not have this as number one on your differential.  She does not have fever or a white count and has relatively normal vital signs, therefore she is not uroseptic.  ITP does not have the hemolytic anemia that she has.  The patient very well could have viral meningitis towards the top of your differential, but Parvovirus B19 causes a pancytopenia and she has a normal white count.  Catastrophic anti-phospholipid syndrome would present similar to this as it causes widespread microvascular and macrovascular changes and this should be on your differential as it is often confused with TTP-HUS.  It would be too early to tell as the first lab value to help differentiate PTT (normal value in HUS-TTP and elevated in anti-phospholipid syndrome) is not back yet.  Fortunately, the initial ED management is the same.

2)    A. Peripheral Smear

a

Peripheral blood smear from a patient with a microangiopathic hemolytic anemia with marked red cell fragmentation. The smear shows multiple helmet cells (small black arrows), other fragmented red cells (large black arrow); microspherocytes are also seen (blue arrows). The platelet number is reduced; the large platelet in the center (red arrow) suggests that the thrombocytopenia is due to enhanced destruction. Courtesy of Carola von Kapff, SH (ASCP).

  • Although there are a plethora of blood tests you should send off, the test that is most likely to confirm the diagnosis is a peripheral blood smear.  This test will come back as soon as you or the hematologist looks at it and will change your diagnosis.
  • Tests that I sent off for Heme/Onc

Test    Value
CBC    Anemia, low platelet count, normal WBC or increased with normal differential
Electrolytes    Elevated BUN/Cr
Coagulation    Normal
UA    Blood in urine, RBC casts
LFTs    elevated indirect Bilirubin/ total Bilirubin
Reticulocyte count    Increased
LDH/Uric Acid    Severely Elevated
ADAMTS-13    Increased activity
DIC panel     Fibrinogen and FSPs normal
Coombs’ Test (direct and indirect)    Negative
Hemoglobin Electrophoresis     Normal
Immunoglobulins A, G, E, M    Elevated IgG
Epstein-Barr Panel    Normal
Lupus Panel    Normal

3)    B. High dose prednisone, pRBCs, FFP while awaiting Plasma Exchange Transfusion

  • The initial management, while awaiting definitive treatment (Plasma Exchange Transfusion) is high dose prednisone 1 to 2 mg/kg.
  • Transfusion of pRBCs is indicated in those with angina, CHF, mental status changes and hypoxia
  • Transfusion of FFP is indicated if there is an anticipated delay in arranging Plasma Exchange (i.e., transferring to a tertiary care center)
  • Supportive care is always indicated
  • DO NOT, under any circumstances GIVE PLATELETS! This is a consumptive coagulopathy and giving platelets will make it worse.  EGDT. Methylprednisolone and IVIG are indicated for ITP.

Patient’s Hospital Course:
Patient was admitted to the MICU for Plasma Exchange Transfusion 1.5 times plasma volume twice daily.  The patient neurological status fluctuated and she had neuroimaging done that was negative for any acute neurological process.  A renal ultrasound showed normal renal architecture.

The patient’s clinical condition improved on day of admission #3, then her mental status deteriorated again on day #5, where repeat imaging was done and the MRI showed multiple focus of infarct with the largest focus in the posterior medial aspect of the right temporal lobe.  A cardiac echo was done and showed no evidence of thrombus.

On hospital day 8 the patient became febrile and IV Ceftriaxone IV was started and cultures were sent.  The femoral pheresis catheter was replaced with an IJ catheter on day 9 the blood and urine cultures grew E. coli sensitive to Ceftriaxone.

The patient platelet count slowly recovered over the next few days but was still below 150 so it was decided that the patient received steroids (Decadron 36 mg PO q12h).

The patient remained on therapy for E. Coli urosepsis for 10 days, showed much clinical improvement and her platelet count raised above 150 on hospital day #18.

On hospital day #20 the patient developed abdominal pain and elevated BP, so steroids were discontinued with clinical improvement.

The patient was discharged on hospital day #22 with pheresis QOD as an outpatient.

The patient had her R IJ catheter removed on post-ED visit day #56.   The patient is doing better with no relapse as of post-ED visit day #85.

Clinical Pearls:

  • CLINICAL DIAGNOSIS of a MEDICAL EMERGENCY!
  • MAHA, TCP, fever, neuro, renal
  • Rarely all five are present (1/3)
  • Don’t give platelets.
  • Transfer out as soon as possible with steroids and FFP hanging.

This case discussion presented by Rob Klever, MD

Intern Report Case 1.8

intern-report

Presented by Rob Klever, MD

HPI
15 year-old female with a past medical history for asthma, who presents to the ED for a headache, myalagias and anorexia of two days duration.  She states that her headache is constant, located bilaterally frontal and of aching quality, relieved by laying down, worsened with movement and has intermittent photophobia. She reports last week that she a had a ‘stuffy nose’ and had one episode of diarrhea and vomiting.

Her grandmother states that took her to the pediatrician five days ago who diagnosed her with viral illness and gave her a prescription for amoxicillin that she took for two days then stopped because she had felt better before developing the headache.

ROS
Patient states that she as a mildly sore neck, but no stiffness.  Pt reports feeling malaised.

Patient denies any fevers, chills, nausea, vomiting, cough, congestion, wheezing, shortness of breath, chest pain, weakness, numbness or tingling in any of her extremities, constipation, diarrhea then the aforementioned week before, changes in bowel or bladder habits.

PMHx
Asthma, currently well controlled on no medications.
Medications: Albuterol prn
Allergies: NKDA

Social Hx
Patient states that several people in her church youth group have been sick lately, but denies any recent travel.
She lives at home with her grandmother and does well at school as a sophomore.
She denies any alcohol, tobacco and drug use.
She reports no sexual history and states last menstrual period was two weeks ago lasting normal duration and volume.

Family Hx
Positive for migraine headaches, negative for sickle cell and diabetes.

Physical Exam:
VS: Temp: 36.6C; HR 84; RR 24; BP 109/71; Wt 69.4 kilo
General: 15 year female who appears stated age.
Eyes: PERRLA, EOMI, sclera icteric, conjuctiva pale, fundoscopic exam shows sharp disc margins, no evidence of papillaedema.
Ears: TM clear
Tonsils: tonsils bilaterally 1+; no evidence of erythema, edema or exudates
Neck: soft, supple, no evidence of meningsmus.  No Kernig’s or Brudzinki’s sign present. Trachea midline.
Cardiac: RRR s1,s2; no m/r/g
Lungs: CTA B
Abdomen: soft, NTND, no evidence of HSM, no rebound, no guarding
Extremities: Patient moves all extremities spontaneously, normal muscle strength and tone.
Neuro exam: Patient has normal gait and station; patient has normal strength and reflexes in all 4 extremities.  CN II thru XII intact.
Skin: Warm, dry and well perfused.  Good skin turgor. No evidence of rashes, petechiae or bruises.  There is palmar pallor present.

Initial Lab Values:
CBC: WBC: 13.0; H/H 4.1/13.4; Plt 8
Na/K/Cl/CO2/BUN/Cr/Glu: 139/4.3/102/23/17/1.5/123
UA: Cloudy, Amber, SG 1.014, pH 5.5, 3+ Blood, 1+ protein, negative nitrite, trace leukocyte esterase, > 100 RBCs, 5-10 WBC, 2-5 RBC casts, 2+ bacteria
Urine β-HcG: Negative

Questions:

1)    Given the history and initial lab values, what is the most likely diagnosis?
a.    Urosepsis with associated DIC
b.    Idiopathic Thrombocytopenic Purpura
c.    Viral Meningitis caused by Parvovirus B19
d.    Catastrophic anti-phospholipid syndrome
e.    Thrombotic Thrombocytopenic Purpura

2)    What lab test do you want to order to confirm the diagnosis?
a.    Aerobic and Anaerobic Blood Cultures
b.    Hemoglobin Electrophoresis
c.    Lumbar Puncture
d.    Peripheral Smear
e.    PT/PTT/INR; D-dimer; Fibrinogen, Fibrinogen Split Products

3)    What is your initial ED management?
a.    Transfusion of pRBCs and Platelets
b.    High dose prednisone, pRBCs, FFP while awaiting Plasma Exchange Transfusion
c.    Early Goal Directed Therapy (Fluids, Antibiotics, pRBCs)
d.    Early intubation, Dialysis, Fluid Bolus, Platelets, Steroids, Broad-spectrum antibiotics
e.    Give methylprednisolone and IVIG

Please submit your answers to the questions in the “leave a reply” box or click on the “comments” link.  Your submission will not immediately post.  Answers with a case discussion will post on Friday.  If you have any difficulty, please contact the site administrator at arosh@med.wayne.edu. Thank you for participating in Receiving’s: Intern Report.

Intern Report Case Discussion 1.7

intern-report

Presented by Richard Gordon, MD

CC
“My chest hurts”

HPI
30 year old AAM presents to ED with 2 day history of worsening sharp chest pain located over the anterior/lateral right ribs.  Patient states the pain is 8/10 in intensity, non-radiating, and exacerbated with deep breathing/coughing.  No obvious alleviating factors.  Patient has never experienced this kind of pain in the past. Patient also complains of mild shortness of breath.  The patient states that he has had a dry cough for the last 4 days without any measured fever, but has felt warm.   No recent travel, no history of DVT in the patient/family, and no history of hypercoagulability. No nausea, vomiting, or abdominal pain. Review of CIS shows the patient was in the ED 7 days ago for “sickle pain” and was treated with 2 rounds of morphine sulfate 10 mg IVP, Benadryl 50 mg IVP, and one liter bolus of normal saline, and subsequently discharged home with pain under control.
PMH: Sickle cell SS, Asthma

PSH: No previous surgery

FH: Mother died at 65 MI. Father died at 62 CVA.  Brother alive 37 HTN, asthma, sickle cell trait. Sister alive 35 sickle cell anemia SS, asthma.

SH: Denies smoking, drinking, or use of illicit drugs.

Meds: Albuterol inhaler 2 puffs PRN for SOB.  Advair Diskus 250/50 inhaled BID. Morphine sulfate controlled release 100 mg BID.  Morphine sulfate instant release 30 mg 1-2 tab Q3H PRN for pain.

All: NKDA

PE:
Vitals:  BP:140/90    HR:115     RR:25     T:39.0     Sat:89% room air

General: Alert and oriented X3. Upright in stretcher answering questions appropriately. However, anxious appearing and looks uncomfortable breathing with accessory muscles, speaking in partial sentences.

HEENT: Head is normocephalic and atraumatic. Pupils equal and reactive to light. Extraocular movements intact. There is scleral icterus. Nares have no discharge. Oropharynx  has moist mucus membranes, no exudates, no erythema. Neck is supple with no JVD, trachea midline, no adenopathy.

Chest Wall: Reproducible chest pain with palpation of ribs bilateral left greater than right.  Reproducible parasternal tenderness.  No crepitus.
Cardiac:  S1S2 regular and tachycardic.  No murmus, rubs or gallops.

Lungs: Good air entry bilateral, end expiratory wheeze, prolonged expiratory phase. Basilar rales present.  No ronchi.

Abdomen: Bowel sounds present, nontender to palpation, nondistended, no masses, no organomegaly.

Extremities: Moves all four with full Range of motion. No asymmetric swelling or erythema. 2+ distal pulses. Calves nontender to palpation.

Skin: No jaundice. No rashes. No diaphoresis

Neuro: Alert and oriented X3. Pupils equal and reactive to light. External ocular muscles intact. No facial asymmetry. 5/5 strength all 4 extremities. Walks with normal gait. No obvious sensory deficits.

Lab Results:

ABG on room air:  7.45/59/30/16/89%

HbG: 8.5 Baseline HbG 9.5

WBC: 15

Lytes: Na-140 K-5 Cl-100 HCO3-15 BUN-18 Cre-0.8
Diagnostics:

12 lead ECG shows sinus tachycardia at rate of 110.

Chest PA shows middle lobe infiltrate.

12
CT chest with PE protocol: No pulmonary embolus, infiltrates right middle and lower lobe.

Course in ED
Patient immediately placed on non-rebreather with saturation rapidly increasing to 100%.  3 doses of albuterol and atrovent via nebulizer were administered with improvement of tachypnea and wheezing.  Patient now maintiaing 94-96% 4L NC breathing more comfortably.  IV established with 1 liter normal saline bolus followed by 1.5 maintenance.  Blood cultures X2 sent, followed by,  IV doxycycline and ceftriaxone administration.  Morphine 10mg with Benadryl 50mg and titrated to pain control.   Patient was type and crossed followed by transfusion with 2 units of blood.  Saturation again improved 96-98% on 2 liters.  Patient admitted to hematology oncology service.

Discussion

1.    Which of the following is NOT considered to be one of the clinical diagnostic criteria for acute chest syndrome in a patient with sickle cell disease?
a)    chest pain and hypoxia
b)    new pulmonary infiltrate(s) on chest x-ray
c)    recent sickle cell pain crisis
d)    tachypnea, wheezing, or cough
e)    temperature > 38.5

There is no current laboratory or radiographic finding to provide definitive diagnosis of acute chest syndrome.  The diagnosis is made clinically with one or more of the following: chest pain, temperature greater than 38.5, tachypnea, wheezing, cough, appearance of increased work of breathing, or hypoxemia. AND new pulmonary infiltrate found on chest radiograph involving at least one complete lung segment that is not consistent with the appearance of atelectasis.

C) Though, it is common for a sickle pain crisis to have occurred prior (usually about 2 days) to onset of acute chest syndrome, it is not currently one of the accepted diagnostic criteria.

2.    Which of the following statements related to acute chest syndrome in sickle cell anemia is correct?
a)    bronchodilators have no role in the acute treatment.
b)    most common chest x-ray finding is new infiltrate in bilateral upper lobes.
c)    only exchange transfusion provides benefit.

d)    pulmonary infection is rarely the inciting cause.

e)    transfusion of packed red blood cells can significantly improve the patient’s condition.

A) Studies suggest that patients with sickle cell disease have increased airway reactivity.  In addition to this, increased airway reactivity further compounds the problem of sickle cell anemia secondary to hypoxia.  With this in mind, it is recommended inhaled beta agonist therapy be administered in all patients whom may have acute chest syndrome, even those with no wheezing.  B) The most common x-ray finding in acute chest syndrome is bilateral lower lobe infiltrates.  D) In a large multicenter study it was found through bronchoalveolar lavage the second most common inciting event of acute chest syndrome is infection. Most commonly Chlamydia pneumoniae followed by Mycoplasma. C) Exchange transfusion can be reserved for those with a PaO2 less than 70 and refractory to supplemental oxygen. E) Simple transfusion does provide a risk of increasing the blood viscosity and further exacerbating the vaso occlusive event (particularly to levels greater than 10). However, studies show similar improvement in oxygenation with both simple and exchange transfusion.

3.    Which of the following statements regarding acute chest syndrome is INCORRECT?
a)    acute chest syndrome is a leading cause of hospital admission and mortality in sickle cell patients.
b)    adequate pain control and incentive spirometry are important adjuncts to therapy.
c)    choice of antibiotic should cover for atypical and encapsulated organisems.
d)    fat embolism is a leading cause.
e)    hydration at 2-2.5 times the maintenance fluid requirement is indicated for treatment.

A) Statistically, acute chest syndrome is the leading cause of mortality in those with sickle cell anemia.  In terms of illness requiring admission acute chest syndrome is second only to acute pain crisis.  B) Pain control and incentive spirometry is an excellent adjunct to managing the acute chest patient. Splinting leads to poor ventilation which raises risk for atelectasis, hypoxia, and secondary infection.  However, caution should be used as over medication can lead to poor respiratory drive and therefore poor ventilation as well.   Some studies suggest Non-invasive Positive Pressure Ventilation is better tolerated with better outcomes. C) Pulmonary fat embolism and infection are believed to precipitate most cases of acute chest syndrome.  With regards to infection Chlamydia pneumoniae is the most common organism found followed by Mycoplasma.  It is also important to keep in mind that sickle patients can have a poor functioning spleen which increases risk for infection by encapsulated organisms.  Therefore it is important to cover both atypical and encapsulated organisms in a patient with acute chest syndrome.  D) Pulmonary fat embolism accounts for up to 25% of acute chest syndrome cases. Intramedullary bone infarction is believed to be the source of pulmonary fat embolism.  Free fatty acid associated enzymes (eg. Phospholipase A) lead to pulmonary and lung parenchyma damage.  E) Intravenous fluid therapy should be used with caution.  Bolus should be reserved for those that are hypotensive.   Greater than one and a half times the fluid maintenance rate rarely (if ever) should be considered for fluid resuscitation.   Over hydration provides a serious risk for iatrogenic pulmonary edema.

Pearls:

  • A patient with history of sickle cell anemia that presents with cardiopulmonary symptoms think acute chest syndrome.  If new infiltrates on x-ray plus above symptoms treat for acute chest syndrome.
  • Administer inhaled beta agonist even with no signs of reactive airway disease.
  • Low threshold for transfusion. Geared towards clinical improvement as opposed to hemoglobin correction.  Important to not exceed hemoglobin of 10 as to avoid hyper viscosity and worsening of pain crisis. Exchange transfusion reserved for PaO2 less than 70 refractory to supplemental oxygen.
  • If emergent exchange transfusion unavailable may try the following:

1. phlebotomize 500ml

2. infuse 300ml normal saline

3. phlebotomize 500ml

4. infuse 4 units packed red blood cells.

  • Pain control is important but not too much! Incentive spirometry also a good adjunct. Non-invasive positive pressure ventilation if patient is still splinting.  For patients on a vent avoid PaO2 much higher than 100 as this can suppress erythropoiesis.
  • Cover for atypical and encapsulated organisms.

This case discussion presented by Richard Gordon, MD

Intern Report Case 1.7

intern-report

Presented by Richard Gordon, MD

CC
“My chest hurts”

HPI
30 year old AAM presents to ED with 2 day history of worsening sharp chest pain located over the anterior/lateral right ribs.  Patient states the pain is 8/10 in intensity, non-radiating, and exacerbated with deep breathing/coughing.  No obvious alleviating factors.  Patient has never experienced this kind of pain in the past. Patient also complains of mild shortness of breath.  The patient states that he has had a dry cough for the last 4 days without any measured fever, but has felt warm.   No recent travel, no history of DVT in the patient/family, and no history of hypercoagulability. No nausea, vomiting, or abdominal pain. Review of CIS shows the patient was in the ED 7 days ago for “sickle pain” and was treated with 2 rounds of morphine sulfate 10 mg IVP, Benadryl 50 mg IVP, and one liter bolus of normal saline, and subsequently discharged home with pain under control.
PMH: Sickle cell SS, Asthma

PSH: No previous surgery

FH: Mother died at 65 MI. Father died at 62 CVA.  Brother alive 37 HTN, asthma, sickle cell trait. Sister alive 35 sickle cell anemia SS, asthma.

SH: Denies smoking, drinking, or use of illicit drugs.

Meds: Albuterol inhaler 2 puffs PRN for SOB.  Advair Diskus 250/50 inhaled BID. Morphine sulfate controlled release 100 mg BID.  Morphine sulfate instant release 30 mg 1-2 tab Q3H PRN for pain.

All: NKDA

PE:
Vitals:  BP:140/90    HR:115     RR:25     T:39.0     Sat:89% room air

General: Alert and oriented X3. Upright in stretcher answering questions appropriately. However, anxious appearing and looks uncomfortable breathing with accessory muscles, speaking in partial sentences.

HEENT: Head is normocephalic and atraumatic. Pupils equal and reactive to light. Extraocular movements intact. There is scleral icterus. Nares have no discharge. Oropharynx  has moist mucus membranes, no exudates, no erythema. Neck is supple with no JVD, trachea midline, no adenopathy.

Chest Wall: Reproducible chest pain with palpation of ribs bilateral left greater than right.  Reproducible parasternal tenderness.  No crepitus.
Cardiac:  S1S2 regular and tachycardic.  No murmus, rubs or gallops.

Lungs: Good air entry bilateral, end expiratory wheeze, prolonged expiratory phase. Basilar rales present.  No ronchi.

Abdomen: Bowel sounds present, nontender to palpation, nondistended, no masses, no organomegaly.

Extremities: Moves all four with full Range of motion. No asymmetric swelling or erythema. 2+ distal pulses. Calves nontender to palpation.

Skin: No jaundice. No rashes. No diaphoresis

Neuro: Alert and oriented X3. Pupils equal and reactive to light. External ocular muscles intact. No facial asymmetry. 5/5 strength all 4 extremities. Walks with normal gait. No obvious sensory deficits.

Lab Results:

ABG on room air:  7.45/59/30/16/89%

HbG: 8.5 Baseline HbG 9.5

WBC: 15

Lytes: Na-140 K-5 Cl-100 HCO3-15 BUN-18 Cre-0.8
Diagnostics:

12 lead ECG shows sinus tachycardia at rate of 110.

Chest PA shows middle lobe infiltrate.

12
CT chest with PE protocol: No pulmonary embolus, infiltrates right middle and lower lobe.

Course in ED
Patient immediately placed on non-rebreather with saturation rapidly increasing to 100%.  3 doses of albuterol and atrovent via nebulizer were administered with improvement of tachypnea and wheezing.  Patient now maintiaing 94-96% 4L NC breathing more comfortably.  IV established with 1 liter normal saline bolus followed by 1.5 maintenance.  Blood cultures X2 sent, followed by,  IV doxycycline and ceftriaxone administration.  Morphine 10mg with Benadryl 50mg and titrated to pain control.   Patient was type and crossed followed by transfusion with 2 units of blood.  Saturation again improved 96-98% on 2 liters.  Patient admitted to hematology oncology service.

Questions:

1.    Which of the following is NOT considered to be one of the clinical diagnostic criteria for acute chest syndrome in a patient with sickle cell disease?
a)    chest pain and hypoxia
b)    new pulmonary infiltrate(s) on chest x-ray
c)    recent sickle cell pain crisis
d)    tachypnea, wheezing, or cough
e)    temperature > 38.5

2.    Which of the following statements related to acute chest syndrome in sickle cell anemia is correct?
a)    bronchodilators have no role in the acute treatment.
b)    most common chest x-ray finding is new infiltrate in bilateral upper lobes.
c)    only exchange transfusion provides benefit.
d)    pulmonary infection is rarely the inciting cause.
e)    transfusion of packed red blood cells can significantly improve the patient’s condition.

3.    Which of the following statements regarding acute chest syndrome is INCORRECT?
a)    acute chest syndrome is a leading cause of hospital admission and mortality in sickle cell patients.
b)    adequate pain control and incentive spirometry are important adjuncts to therapy.
c)    choice of antibiotic should cover for atypical and encapsulated organisms.
d)    fat embolism is a leading cause.
e)    hydration at 2-2.5 times the maintenance fluid requirement is indicated for treatment.

Please submit your answers to the questions in the “leave a reply” box or click on the “comments” link.  Your submission will not immediately post.  Answers with a case discussion will post on Friday.  If you have any difficulty, please contact the site administrator at arosh@med.wayne.edu. Thank you for participating in Receiving’s: Intern Report.