MOC November 2014: A Harrowing Tale of Hernias, Methadone, and Abdominal Pain

Patient is a 58 year old who presents complaining of abdominal pain. He reports the pain has been present for a month, initially intermittent and now more persistent. It started as back discomfort and has evolved into bilateral flank pain radiating to his umbilicus. His symptoms seem worse he takes a deep breath. He has had a previous umbilical hernia repair but no other abdominal surgeries. He was seen at an outside facility for this same pain twice in the past 7 days. He reports that they did not do labs or imaging but diagnosed him with constipation and sent him on prophylaxis. He's had 2 large bowel movements since that visit but has not had any change in his symptoms.

He denies any fevers or chills, vomiting or diarrhea and has not had any urinary symptoms including frequency or dysuria. He does not have any history of gastric ulcer or pancreatitis nor does he have symptoms of early satiety.

His past history is significant for a previous umbilical hernia repair. He also has a distant history of IV heroin abuse and currently takes methadone daily. He reports no IV heroin use for the past year.

Medications: Methadone 110 mg daily, Seroquel 250 mg QHS

Allergies: NKDA

Physical Exam:

Vital signs: BP 135/80  HR 90  RR 18  temp 98 F

General: Male, generally looks mildly uncomfortable. Appears stated age and in appropriate dress and hygiene

Cardiovascular exam: unremarkable with no murmur

Pulmonary exam: unremarkable with clear lung sounds and normal respiratory rate

Abdominal exam: large midline incision that is old and well-healed, he has a small easily reducible recurrent hernia. He has no focal tenderness though there is some minimal distention of his abdomen with normal bowel sounds.

Skin exam: Unremarkable without evidence of infection or injection sites

Neuro: Symmetric motor strength and sensation diffusely, alert and oriented

- - - - -

Differential diagnoses: Colitis, UTI, urinary retention, pancreatitis, hepatitis, gastritis, intra-abdominal mass, symptomatic umbilical hernia.

Work up:
WBC 3.8. Electrolytes, liver, lipase, and urine are all normal.

Care everywhere accessed and there was a plain film at the outside facility showing moderate amount of stool is abdominal x-ray, unremarkable labs and no definitive diagnosis. 

Question: With negative exam and unremarkable labs, is more imaging indicated?

- - - - -

Imaging:

Abdominal CT results:
Prominent disc space narrowing at T9-10 with irregularity and some sclerosis and prominent spurring of the adjacent endplates.  This is associated with some fullness of the adjoining paraspinal soft tissues.  Findings are nonspecific.  A underlying discitis or disc space infection are not excluded on the basis of this exam.  Further clinical correlation is recommended with consideration for a MRI of the thoracic spine if warranted clinically.

MRI thoracic spine:
Acute discitis/osteomyelitis at the T9-10 interspace with epidural spread of infection and phlegmon formation extending from the level of T8-9 through T10-11.  This epidural component results in severe spinal canal narrowing at the level of T9-10.  Abnormal enhancement extends into the bilateral neural foramina with loss of the normal perineural fat.  There is paravertebral soft tissue extension of infection from the level of T8-T11 with a likely small abscess within the left paravertebral soft tissues at the level of the T9 body.

The patient later disclosed, to the hospitalists, that he had been injecting his methadone into his veins for the past 2 months...

- - - - -

Questions

1. What percent of patients with osteomyelitis of the spine have an elevated ESR

    a. 40%

    b. 50%

    c. 70%

    d. 80%

2. True or false: Though the most common bacteria associated with osteomyelitis of the spine is Staph aureus, Pseudomonas aeruginosa is often found in patients whose infection is likely caused by IV injections.

3. What is the recommended timing for initiation of antibiotics?

    a. Immediately upon suspicion of diagnosis

    b. Once biopsy cultures have resulted so therapy can be directed specific to the infectious agent

    c. Not until after biopsy so as not to alter biopsy results

    d. Once confirmation is made via advanced imaging

4. All of these are considered causes of vertebral osteomyelitis. Which is by far the most common?

    a. Hematogenous spread from a distant site or focus of infection

    b. Direct inoculation from trauma or spinal surgery

    c. Contiguous spread from adjacent soft tissue infection

MOC August 2014: IRIS

History

It's the season of sub-zero weather when you (and your parka) meet an ambulance coming in. 

Patient is a pleasant 50-year-old female with a pertinent past medical history that includes breast cancer, history of prosthestic heart valve (on Coumadin), mitral regurgitation, and SVT who presents to the emergency department today for evaluation of shortness of breath. She is currently on chemotherapy for breast cancer and her last treatment was 6 days ago. She is actually discontinuing treatments due to adverse reactions.

No history of HIV.  Denies associated symptoms such as fever, chills, cough, chest pain, nausea, vomiting, abdominal pain.  No urinary symptoms.  No headache or neck pain.

Of note, patient was recently in the ED (3 days ago) for evaluation of SVT and had an ablation at that time.

Social History

Single, part time caregiver.  Has never smoked.  Drinks approximately 8 beverage of hard alcohol per week.  Denies illicit drug use.

Allergies

Bactrim; Mold extracts; and Pollen extracts

Medications

Reviewed and non-contributory with exception of chemotherapy agents and Coumadin.

Physical Exam

Vital Signs: Temp 97.9°F, HR 78, BP 113/65, SpO2 100% on room air, Wt: 95 kg, Ht 167 cm

Patient is alert and oriented x3.  She has a mechanical heart sound, but no murmur.  Has mild respiratory distress, speaking in 3 word phrases.  No wheezes or crackles.  No pedal edema.  Abdomen is soft and nontender.  Port-a-cath in place in right upper chest.  Remainder of exam is unremarkable.

Differential diagnosis

CHF, SIRS, Sepsis, Pneumonia, COPD, ACS, PE, others.

Diagnostic Testing

EKG

HR 107

Sinus Tachycardia

Otherwise unremarkable

Chest X-ray

No acute consolidations.  Prosthetic cardiac valve and Port-A-Cath visualized.  Pulmonary vasculature within normal limits. 

Labs

CBC - WBC 13.7, Hgb 8.4, Plt 179; elevated bands

BMP remarkable only for creatinine of 2.13 (new from previous labs)

BNP 1748

INR 4.6

Troponin 0.899

Urine negative

Lactate pending

Updates

You are notified that the patient’s temperature is now 104.6°F.  Lactate is ordered and elevated at 2.6.

Next steps

What are you thinking – update to differential?

            Add: IRIS, endocarditis.

Any treatments you would start immediately in the ED at this point?

            Antibiotics?  Lasix?  Heparin?  Steroids?

What is your plan?

            Admit and let the hospitalist deal with it!

What is IRIS?

"Immune Reconstitution Inflammatory Syndrome"

This is a syndrome in which there is paradoxical worsening of pre-existing infections in certain situations - namely initiation of HAART therapy for HIV.  This can also happen with corticosteroid withdrawal, chemotherapy discontinuation, recovery of neutropenia after cytotoxic chemotherapy, and other situations.  The most common and definition of the syndrome is when HAART is initiated in HIV infected patients that have an opportunistic infection that they are being treated for, such as CMV, Pneumocystis, cryptococcal, or others.

Basically what happens is that the immune function improves too rapidly, causing systemic (or local) inflammatory reactions.  This reaction can range from self-limited (most of the time) to fatal.

Diagnostic Criteria

•   Presence of AIDS with low pretreatment CD4 count.

•   Positive virologic and immunologic response to HAART.

•   Absence of evidence of drug-resistant infection, bacterial superinfection, drug allergy or adverse reaction, patient non-compliance, or reduced drug levels.

•   Presence of clinical manifestations consistent with an inflammatory condition.

•   Association between HAART initiation (or recovery of neutropenia after chemotherapy in our case) and onset of clinical features of illness.

•   It is a diagnosis of exclusion.

Leading pathogens: Mycobacterium tuberculosis or avium, cytomegalovirus, cryptococcus, pneumocystis, herpes simplex, hepatitis B, human herpes virus 8.

Clinical Manifestations

Vary widely.  Only about 50% of patients will develop fever.  Often related to whatever the underlying infection is.  Onset is typically 12-45 days after initiation of HAART.

Management

Treat the infection, but recognizing that the timing is related to HAART, chemo, or other cause is key to management for the future.  There really is no prevention.  Anti-inflammatory agents such as corticosteroids or NSAIDs can be helpful in decreasing symptoms.

Outcome

Our patient ended up being diagnosed with severe sepsis caused by probable endocarditis.  Blood cultures grew out staph aureus.  She had a normal Echocardiogram 7 days before admission, and the day of admission had a thickened mechanical valve (no gross vegetation).  She may not have actually had IRIS, but I had discussed the patient with the hospitalist, who asked me then to call cardiology and infectious disease and he was the one who brought up the possibility.  I had never heard of it so I looked it up.  Patient was given antibiotics in the ED. She was admitted to the ICU and had a 7 day hospital stay and was discharged to a TCU.

Questions

1. What does IRIS stand for?

a.    Irritational Radiation Idiopathic Syndrome

b.    Immune Reconstitution Inflammatory Syndrome

c.    It Rules In Sepsis

d.    Immunologic Restoration  Iatrogenic Syndrome

      2. Which of the following is another example of a situation in which a patient can develop IRIS when not on HAART or HIV positive?

a.    Recovery of neutropenia after cytotoxic chemotherapy

b.    Initiation of corticosteroid therapy

c.    Bacterial superinfection

d.    Initiation of therapy for Hepatitis C

      3. Which of the following is NOT a sign or symptom of bacterial endocarditis?

a.    New Murmur

b.    Petechiae

c.    Koplik Spots

d.    Splinter Hemorrhages

      4. What percentage of patients develop fever with IRIS?

a.    5%

b.    25%

c.    50%

d.    80%

      5. Which of the following is NOT one of the diagnostic criteria for IRIS?

a.    Presence of clinical manifestations consistent with an inflammatory condition.

b.    Absence of drug-resistent infection, bacterial superinfection, drug allergy or adverse reaction, patient non-compliance, or reduced drug levels.

c.    Association between HAART initiation and onset of clinical features of illness.

d.    Positive IRIS antigen

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

Answers

     B

     A

     C

     C

     D

MOC June 2014: Young and confused

You just arrived for your 4pm shift, when you hear overhead, “Ambulance to Room 1 in 5 minutes, STAB team room 1 in 5 minutes”.  You head to the room to prepare.  39 year old female coming by EMS, syncopal episode with head trauma now confused, though airway intact, vitals stable.

EMS Arrives:  39 year old female with no significant PMHx, was at Pickerel Lake for a picnic with family when she stated she didn’t feel well, stood up and was walking towards the bathroom.  Was walking up a concrete staircase then syncopized, falling with impact to her head and left side.  +Brief LOC, no seizure activity per family, ambulatory shortly after, however seemed confused and not making sense.  Backboarded with C-collar at EMS arrival.  Accucheck 125.  Negative stroke screen, alert, but limited verbal output, complaining of headache unable to obtain further history.  12 lead with sinus tach.  T 37 C P 110s  BP 128/80  R 18  SpO2 100%.  1 P IV in place, no interventions en route.

HPI: Patient is intermittently moaning, speaks few words but cannot provide additional history.  No prior visits in EMR.

- - - - -

1-- Should this patient be a trauma team activation?

United criteria for Level 2 trauma activation:

 - GCS 12-14 (not associated with alcohol or other substances)

 - >/= 20% BSA burns

 - Fall >20 feet or 2 times the height of child

 - Auto vs pedestrian with significant impact

 - Ejection from auto or other moving vehicle

 - High speed MVC with severe single injury or multiple system injuries

 - Death in same compartment

 - Pregnant trauma > 16 weeks

 - ED MD discretion

- - - - -

Exam:

Vitals: T 37.3 C  P 120  BP 140/90  R 18  SpO2 97%RA
Gen: Adult female, laying in bed, opens eyes and looks around, moans

HEENT: Small hematoma with overlying abrasion on left occiput, Normocephalic, PERRL, EOMI, Oropharynx clear, no signs of facial trauma

Neck: Supple, C-collar in place, trachea midline, no JVD, no signs of trauma

Cardiac: Tachycardiac with regular rhythm, no m/r/g

Pulm: Clear and equal, no tachypnea

Abdm: Soft, nondistended, no reaction to palpation

Extrem: Warm, well perfused, atraumatic

Neuro: Alert, minimal verbal response with few words spoken, no overt dysarthria, no facial droop, moves all extremities spontaneously, follows commands (opens eyes/squeezes hands)

Skin: Outside of scalp abrasion/hematoma, no other signs of trauma nor skin changes

Bedside eFAST negative

- - - - -

2-- What is their GCS?  Do they need airway control?

GCS 13 = motor 6 + verbal 3 + ocular 4

Although altered, appear to be protecting their airway

3-- Differential diagnosis?

Arrhythmia, CVA, Seizure, Hypoglycemia, Hypovolemia, Vasovagal, Valvular disease, Heat stroke, ACS, SAH, ICH, TBI, Overdose and others

4-- What imaging/labs do you order?

Initial orders included:
 - Portable CXR, CT/CTA head/neck, CT cspine

 - iSTAT creatinine

 - CBC, Comp, Troponin, PT/PTT, Ethanol, ASA, Tylenol, UA/Upreg

 - EKG

- - - - - 

Portable CXR negative

Patient taken to head CT for planned CT/CTA head/neck, CT C-spine. While in CT reviewing images, the tech informs you iSTAT creatinine is 1.9. CTA canceled.

CT head/C-spine negative

- - - - -

Patient taken back to room 1, EKG with sinus tach & you ask the RN to cath to obtain urine.

Hmm… that doesn’t look right.  You decide to repeat the FAST exam, still negative.  Labs pending.

You walk away to check on another patient when shortly later lab calls with critical values on CBC:

  - HGB           8 

  - Platelets      10

You go back to reassess the patient...

She opens her eyes, states she has a headache. When you ask more questions, she looks around and does not respond, then closes her eyes. Patient squeezes your hands, moves her toes, exam otherwise unchanged, protecting her airway.

Family has just arrived and state she was doing well until 2 days ago, went to Urgent Care for abdominal pain with N/V/D, they thought she was better and no other complaints they were aware of.  No prior med hx, on no meds, NKDA. Smokes cigarettes, drinks socially, no drug use.

- - - - -

5-- Any change in your differential diagnosis? 

Acutely altered patient with fever, tachycardia, presumed new anemia, thrombocytopenia and renal insufficiency:

TTP, HUS, Sepsis +/- DIC, Meningitis, Preeclampsia/HELP, Malignant hypertension, Connective tissue disorders/Systemic Vasculitis, Autoimmune hemolytic anemia, Systemic Malignancy, Overdose

- - - - - 

Remainder of labs return:
 - WBC 11, 75% neutrophils, no bands

 - Hgb 8, microcytic

 - Platelets 10

 - Na 134, Potassium 5, Cl 111, CO2 18, BUN 14, Creat 1.9, Glucose 124

 - AST/ALT/Alk Phos/Alb wnl, TBili 2.7 

 - PT/PTT wnl

 - Troponin 0.050

 - ASA/Tylenol - negative, Ethanol - negative

 - UA +protein, +blood, +LE, >100 RBCs, 5-10 WBCs, no bacteria

 - UPreg - negative   

- - - - -

6-- Further narrowing of the differential?  What additional labs do you consider?  Medications?  Consults?

 - Patient presenting with classic pentad of TTP

 - Add on type & screen, peripheral smear/LDH/indirect Bili to help confirm MAHA, blood cultures, lactate, procalcitonin, retic count

 - Heme/Onc and place catheter placement for plasma exchange

 - Also need to include sepsis in differential, would start broad-spectrum antibiotics and supportive therapy while completing diagnostic workup

- - - - -

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

Thrombotic Thrombocytopenic Purpura, aka TTP:

Rare blood disorder caused by clotting in the microvasculature.  Cause unknown, however thought to be due to abnormally large forms of von Willebrand factor in patient’s plasma, either due to congenital defects, acquired antibodies, release from endothelial injury and others.  The enlarged vWF forms lead to platelet aggregation/microthrombi, which in turns causes consumptive thrombocytopenia.  Microangiopathic hemolytic anemia results due to fragmentation of RBCs as they cross arterioles/capillaries occlude by thrombi.

Microvascular ischemia leads to symptoms/signs involving multiple organ systems.

The “Classic” Pentad of TTP includes: microangiopathic hemolytic anemia, thrombocytopenia, neurologic abnormalities, fever, and renal disease. However it is rare to see all five present.

High index of suspicion for clinical diagnosis is required as treatment is time sensitive.  The mortality rate is >90% if untreated, 10-20% with treatment. Treatment of choice is plasma exchange.

- - - - -

Questions:

1. True/False: At least 3/5 findings in the pentad of TTP are required to establish the diagnosis.

2. Which one of the following explains the etiology of most cases of TTP?

a. Drugs

b. Idiopathic

c. Familial

d. Iatrogenic

e. Paraneoplastic

3. Which one of the following laboratory variables would not be expected in a patient with TTP?

a. Low platelet count

b. Elevated indirect bilirubin level

c. Normal APTT and PT values

d. Normal reticulocytes

e. High serum LDH value

4. If plasma exchange therapy is not available immediately, which one of the following therapeutic options would be best until plasma exchange can be initiated?

a. Platelet transfusion

b. FFP infusions

c. Red blood cell transfusions

d. Hemodialysis

e. Intravenous immunoglobulin

5. True/False: Platelet transfusions are indicated in TTP with a platelet count <10,000.

6. Which one of the following therapeutic or supportive measures is not indicated in the management of TTP?

a. Heparin

b. Red blood cell transfusions

c. Glucocorticoids

d. Plasma exchange

e. Antihypertensive agents

7. Which of the following drugs is not classically associated with TTP?

a. Cyclosporine

b. Clopidogrel

c. Bactrim

d. Tacrolimus
e. Quinine

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

.

Answers:

1. False. TTP is a clinical diagnosis with significant time sensitivity to initiate treatment as well as a high mortality rate if untreated.  Only thrombocytopenia and microangiopathic hemolytic anemia without other clinically apparent etiology is required to establish the diagnosis.

2. b. Idiopathic

3. d. Normal reticulocytes -- Would expect elevated reticulocytes given normal bone marrow response to hemolysis/anemia.  A, B, E all classic due to hemolysis and consumptive thrombocytopenia.  Abnormal PT/PTT levels is suggestive of DIC.  Would expect to see schistocytes on peripheral smear to confirm MAHA.

4. b. FFP infusions -- Risk of FFP infusions alone without plasma exchange is volume overload, particularly if oliguric/anuric or CHF.  If unable to obtain timely plasma exchange, patient should be transferred to definitive care.

5. False.  Platelet transfusions are generally contraindicated in TTP and can lead to significant morbidity due to increased microcirculatory aggregation.  Only indicated in life-threating hemorrhage, which is rare in TTP.

6. a. Heparin

7. c. Bactrim

MOC May 2014: Weekend with Chest Pain

Visit #1: The Saga Begins

You are working on Saturday evening at 7 pm - a time when the word "echo" is interpreted literally by those who perform cardiac stress testing.  

History:

Your patient is 53 year old male nonsmoker who presents with a chief complaint of “it hurts to breath." He describes his pain as sharp and substernal. He says it increases with exertion but is quick to point out that he thinks that is because exertion makes him take deeper breaths. The pain has been present for several days and came on gradually. He says “If I hold really still I have no pain.” 

You assess his cardiac risk: He is sedentary and mildly obese.  He has no known history of diabetes, HTN, or lipid disorder.  His Family History is negative for cardiac disease or PE. 

  

You assess his risk for PE: He denies any recent travel or immobilization.  He also denies leg pain or swelling. He has no personal history of clot.  By Well's criteria he is low risk.  You cannot perform the PERC rule because he is older than 50 years of age. (Shucks) 

He denies fever or chills but has a bit of a dry cough. 

Review of Systems is otherwise negative. 

Vital Signs: 

Temp 99.0, Pulse 92, O2 sat 94% on RA, BP 190/87, RR 18

Physical exam:

General: Speaking in complete sentences, No distress. 

Lungs: normal breath sounds.

CV: Heart sounds normal

Abd: Non-tender, normal bowel sounds, no pulsatile mass.

Extremities: no tenderness, edema or erythema

- - - - -

What is your Differential Diagnosis (you do this every day...sometimes all day)?

• PE
• Atypical angina
• Chest wall pain
• Pneumonia
• Pleurisy
• Anything else???

- - - - -

Cognitive Pause:  You have a patient with risk of age, male, maybe untreated hypertension with chest pain which he clearly describes as pleuritic. He attributes pain to deep breaths. He seems to be a good historian, intelligent with no signs of anxiety.

So you order some tests: 

  

EKG: normal sinus rhythm and no acute t wave findings to suggest ischemia. 

Labs:

WBC                               normal

Hgb                                 normal

Trop (istat)                     negative

D-dimer                          0.9

.
.
.
.
.
.
.
.
.
.
.
.
.
.
.


You can't really ignore that d-dimer... so you get a CT Pulmonary Angiogram...

.
.
.
.
.
.
.
.
.
.
.
.
.
.
.

Interpretation: Two subsegmental Pulmonary Emboli in the distal pulmonary arterial vasculature. 

Disposition: 

You admit your patient to the Hospitalist service.  He is heparinized and started on warfarin. He is ultimately discharged 3 days later. BP to be further evaluated in follow up. No repeat EKG or trop.

As for you, you finish your shift feeling great - you diagnosed a PE - you may have SAVED A LIFE! Mission accomplished. Almost a decade of med school and residency has been put to good use. You rub your tired eyes and drive off into the sunset (in your Lamborghini Aventador, getting 18 mpg on the highway).

 

 - - - - -

Visit #2: the Plot Thickens

You are working ANOTHER WEEKEND!!! It's been 4 days since your patient's discharge, again Saturday evening.

History:

Your patient returns to the Emergency Department. His chief complaint this time: “I am having more blood clots." He reports that the pain never subsided even transiently with anticoagulation. Being an analytical type guy who has been on the internet, he is concerned that his legs were never looked at with ultrasound. The pain is still intermittent and related to deep breaths and exertion. No new symptoms.

Vitals Signs and Physical exam:

Temp 98.0, Pulse 98, O2 sat 96% RA, BP 154/85

Heart, lung and leg exam still normal.

- - - - -

So you order some tests: 

EKG: Slight decrease in amplitude of R waves in V4-6, no Q waves.

Cognitive Pause: Patient concerned about continuing clots, unlikely to be passing more, but clot burden in legs unknown. Adequately anticoagulated. Clinically does not meet criteria for suspicion of further clots or need for IVC filter.  His pain does not strongly suggest cardiac origin but does have subtle EKG changes. Repeat CT pulmonary angio not indicated. Again, combined study of coronary arteries and central pulmonary circulation unavailable. Venous Doppler noninvasive, maybe reassuring. Patient sent for Doppler.

Labs:

Troponin sent...

Radiology is very prompt and lab not so much. 

The patient returns with his negative Doppler result. 

Then Trop results at 2.34

(Trop can be up with PE but clinically he has no vital sign changes suggesting large PE.)

Disposition:

Patient is admitted again, this time to Cardiology. Echo showed left wall motion abnormality and coronary angiogram later showed significant LAD lesion which was successfully stented. EF reduced but clinically no CHF.


.
.
.
.
.
.
.
.
.

Oh. Woah.

- - - - - 

Brief Discussion:

1) How did the timing and availability of testing affect this patient’s workup?

2) A small number of us many years ago learned to calculate the Aa gradient as our best “educated guess” of whether a pt had a PE. Technology progressed by leaps and bounds since then, but has it progressed to the point that it can reveal clinically insignificant pulmonary emboli which divert attention from other causes?

3) Should “missed diagnosis” be added to the downside of super sensitive PE imaging?

We will be discussing a great article about the Sensitivity of PE testing in the upcoming Journal Club. Stay Tuned!

April Mock Online Case: Heartfelt Pregnancy

It's finally spring and despite the Twin's opener and the gorgeous weather, you've hauled yourself into work to save some lives. 

A 43 year old Caucasian female presents to United ED triage complaining of anxiety and hallucinations. She is POD 5 from a scheduled repeat C-section and tubal ligation and was discharged home yesterday. She had no significant complications during this pregnancy and had no complications following her previous two deliveries. While in the hospital after delivery she started developing hallucinations that she described as hearing people talk to her.  Psychiatry was consulted and diagnosed her as "mild delirium of mixed origin, secondary to anesthesia, opioids and sleep deprivation."

She returns to the ED today accompanied by her husband and is roomed in the mental health suite.  She reports worsening hallucinations that are now described as hearing friends or nurses enter her room and ask if she's seen or read certain books or movies. Her husband states he doesn't think she has slept at all since coming home. She has a long standing history of insomnia (and does have a newborn at home) but on further questioning, this is different as she feels she can't lay down as she gets extremely short of breath laying flat.  She denies any new leg swelling, no dyspnea on exertion or feeling short of breath otherwise.

First Vitals:
    BP: 171/101 mmHg   Pulse: 87   Resp: 18    SpO2: 96 %          

Physical Exam with pertinent findings.  
Constitutional: She is oriented to person, place, and time and well-developed, well-nourished, and in no distress. 
HENT:  
Cardiovascular: Normal rate, regular rhythm and normal heart sounds.  
Pulmonary/Chest: Effort normal. Crackles at both lung bases. 
Abdominal: Soft. There is no tenderness. There is no rebound and no guarding. C-section incision well healing. No signs of infection. 
Musculoskeletal: Trace edema bilateral lower extremities.  L>R  
Neurological: She is alert and oriented to person, place, and time. GCS score is 15. 
Skin: Skin is warm and dry. 
Psychiatric: Affect normal.  Speech is clear and fluent but repetitive.  Auditory hallucinations.

What would you do next?

- - - - -

Labs:

Na 141

K 3.3

Cl 111

CO2 19

BUN 9
Cr 0.60

AST 24

ALT 19

Bili total 0.3

AP 104

Trop 0.020

BNP 365

CXR

Bilateral pulmonary infiltrates right > left due to pulmonary edema

ECHO

Normal LV size.

EF 40-45% with mildly reduced global left ventricular systolic function

- - - - -

Patient was transferred to a regular ED room and noted to be severely dyspneic walking the 50 feet between rooms. Lasix 40mg IV and nitro paste 1" administered.  BP improved with these treatments.  Patient noted symptomatic relief while still in the ED.  

She was admitted to the United Hospitalist service with OB and cardiology consulting.  She was managed with lopressor, lisinopril, hydralazine and lasix.  Her weight dropped form 86kg to 78kg over the next two days, and she was discharged on hospital day #3.  Patient was able to sleep while admitted and she had no ongoing hallucinations.  Follow up with cardiology demonstrated complete resolution of her post-partum cardiomyopathy with no residual symptoms.  

- - - - -

Questions:

1.  What is the time period a patient can develop peripartum or post partum cardiomyopathy?

          a. 1 month prior to delivery to 5 months post partum

          b. up to 9 months post partum

          c. any time post partum

          d. 2nd trimester onwards to 1 year post partum

2. What are the risk factors for developing peripartum cardiomyopathy? (choose any/all correct answers)

          - Maternal age >30

          - Multiparity

          - African descent

          - Multiple gestation

          - History of pre-eclampsia, eclampsia or post-partum hypertension

          - Maternal cocaine use

          - Long term oral tocolytic use

3.  True or False? ACE/ARBs are contraindicated for treatment of peripartum cardiomyopathy.

4.  What percentage of women have return to normal LV function?

          a. 95%

          b. none

          c. 20%

          d. 54%

5. True or False? Women with peri/post partum cardiomyopathy cannot reasonably consider a repeat pregnancy after returning to baseline LV function.

Answers:

1. a

2. all of the answers are correct

3. True

4. d, and almost all that recovered to baseline did so within the first 6 months.

5. False