Case of the week COW #10

CC: Nausea and vomiting and “ I think my sugar is low”

HPI: 36-year-old Female with PMH of Diabetes presents to the Emergency Department complaining of multiple episodes of non-bloody, non-bilious vomiting for the past 5 days. Associated symptoms include chills and a mild sore throat. Denies fever, HA, neck pain, chest pain, SOB, abdominal pain, diarrhea or bloody stools. Denies dysuria, hematuria or urinary frequency or urgency. Denies recent travels or sick contacts.   LMP: Currently menstruating

PMH: Diabetes

PSH: C-Section

Meds: None

Allergies: NKDA

Social: Admits to smoking 2 cigarettes per day for the past 10 years. Smokes marijuana daily. Denies alcohol use

 

Physical Exam : 

BP 171/82   HR 82    RR 20     SpO2 100% on RA    Temp 97.8F     108.86 kg

Constitutional: Alert, wake, and in no acute distress. Obese

HEENT: NCAT, pupils PERRLA, neck is supple. Oral mucosa is pink, dry and intact. No lesions. Normal conjuctiva

Respiratory: CTA B/L, no rales, rhonchi, no stridor or wheezing

Cardiac: +S1/S2, regular rate and rhythm, no murmur, rubs or gallop

Abdomen: Soft, with mild tenderness in epigastric area. No rebound or guarding. Normal BS

Neuro: AAO x 3. No focal deficits, moving all four extremities. Steady gate without difficulty.

MSK/Extremities: no edema, tenderness or swelling.

Skin: Moderate ecchymosis overlying RUQ and RUE. Normal moisture. No rash or lesions noted

 

Pertinent Labs:

WBC: 8.4   HGB: 9.3   HCT: 26.8   Platelet: 9L

Na: 136        K: 3.4          Cl: 104        Co2: 26      BUN: 16     Cr: 0.95   Glucose: 109

PT: 14.4   PTT: 28.7     INR: 1.1

Calcium 8.8         Total Bilirubin: 2.8       Alk Phos: 56           AST: 21                 ALT: 12

Lipase: 60

UCG: negative

Urinalysis: Large Blood with negative Nitrites and Leukocyte Esterase without ketones. UA Protein: 100

 Pertinent Images and other tests: Chest X ray: Borderline heart size. NO active disease

Upper Abdominal U/S: Normal Liver and spleen. The spleen measured 10.9 cm in greatest dimension and was homogeneous in echotexture. No focal splenic lesion identified. The liver measured 16.5 cm and appeared normal.

EKG:

 

Working Diagnosis:

Thrombotic Thrombocytopenia Purpura (TTP)

Idiopathic Thrombocytopenic Purpura (ITP)

Hemolytic Uremic Syndrome (HUS)

Anemia due to blood loss

Infection/Sepsis

ED Course: On further questioning, patient states she has been menstruating for 3 weeks now and bleeding is heavier as compared to the previous cycle. In the ED, patient was given NS 0.9% 1000mL IV bolus once, Zofran 4 mg IV once, Reglan 10mg IV once. Type and screen and blood cultures were also sent and patient was admitted to the Medical ICU for thrombocytopenia and anemia.

Hospital Course:

In the Medical ICU, further lab results demonstrated elevated the following:

LDH: 699         Fibrinogen: 410     Haptoglobin: < 10              Troponin 0.44

Blood Cultures: No Growth

Urine Toxicology: Positive for cannabinoids

Hepatitis C antibody: < 0.1

HIV Ag/Ab: Non reactive

In the ICU, patient was given a 125mg bolus of IV Solu-Medrol and then started on 60mg IV every 8 hours. She was transfused 1 Unit of platelet with no response, as the following day, platelets actually dropped to 5.Hematology/Oncology was also consulted. They stated that the occasional schistocytes seen on blood smear with low Haptoglobin levels and elevated reticulocyte count and LDH was suggestive of microangiopathic hemolytic anemia, making TTP a more likely diagnosis. Heme/Onc recommended against any further platelet transfusion and ADAMS 13 levels were sent. On hospital day #3, patient’s LDH levels had increased to 1586 and Troponin was elevated to 1.2 with symptoms of dyspnea. Patient also had worsening anemia as hemoglobin dropped to 7.0, and platelets remained at 9. The same day, Surgery was consulted and patient was transfused 2 Units of PRBs and 2 Units of FFP in preparation for Shiley Catheter insertion for plasmapheresis. Cardiology was also consulted for the elevated troponin, which they attributed to ongoing demand ischemia without any evidence of ACS. Unfortunately, the following night at 1:25 AM and before a Shiley was ever placed, the patient became minimally responsive and Saturating at 90% on RA. Immediately, she became bradycardic and lost pulses. CPR was initiated as patient was simultaneously intubated. Total duration of CPR was 60 minutes. The patient received Epinephrine x 20, Amiodarone 300 mg x 1 and Insulin with 1 amp of D50W, Calcium chloride and Sodium Bicarbonate for Potassium of 6.1 on ABG. Sadly, the patient was pronounced at 2:25AM.

PEARLS : Thrombotic Thrombocytopenic Purpura (TTP)

PENTAD = ‘FAT RN”

  1. Fever (50%)
    • Uncommon if they present early in the disease
    • High fever and chills suggest sepsis, so look for a source of infection.
  2. Thrombocytopenia
    • MAJOR diagnostic criterion
    • Mean platelet of 25, 000 but they reach 5000.
  3. Microangiopathic Hemolytic Anemia
    • MAJOR diagnostic criterion
    • Non-immune hemolysis with schistocytes
    • Results in elevated LDH, Low haptoglobin and high indirect bilirubin
    • Severely elevated LDH has been associated with MI, arrhythmias, shock and heart failure.
  4. Renal Failure
    • Due to renal thrombotic microangiopathy
    • Urinalysis will show mild proteinuria +/- hematuria
    • Acute Rena insufficiency may be present and may require dialysis.
  5. Neurological Symptoms: (Seizure, AMS, HA, coma, hemiplegia, aphasia, etc.)
    • Focal Deficits less prevalent
    • Occurs in 25-60% of patients
    • Symptoms are usually transient and subtle, so you must ask the patient about prior symptoms!

*** KEEP in mind; all features of the PENTAD do NOT to be present at the same time for diagnosis to be made.

Risk Factors

  • Obesity
  • African American race
  • Female
  • Ages 30-50 years
  • HIV/AIDS
  • Rheumatologic/autoimmune disease history

 Clinical Presentation

  • Fatigue, tachycardia, pallor, SOB or chest pain
  • Abdominal pain, back pain, Nausea, vomiting or diarrhea
  • New Onset jaundice and dark colored urine

Physical Exam

  • Diffuse, non-palpable petechial/purpuric rash.

Etiology

  • ADAMTS-13 protease enzyme deficiency
    • 60% of cases
    • Enzyme cleaves von Willebrand factor (vWF) multimers. Without it, excessive platelet aggregation, thrombocytopenia and thrombosis occurs
  • Idiopathic or Secondary Causes
    • 40% of cases
    • (i.e. HIV, malignancy, Infection, Pregnancy, pancreatitis, autoimmune disease, pancreatitis and medications such s Acyclovir, Quinine, Oxymorphoine, Plavix and Tacrolimus)
  • Diagnosis/Lab findings
    • NORMAL PT, PTT and Fibrinogen levels (Unlike in DIC)
    • Thrombocytopenia
    • Anemia and elevated indirect bilirubin
    • A peripheral smear is important for diagnosis, as 100% of patients will have schistocytes present during the course of the disease
    • ADAMTS-13 activity < 10% (normal activity is > 50%)

*** Remember that TTP is a clinical diagnosis. Do NOT delay treatment!

  • Differential Diagnosis
    • Other Causes of Microangiopathic Hemolytic Anemia (MAHA)
      • DIC, HUS, HELLP Syndrome, Malignant Hypertension, Heparin induced thrombocytopenia, Paroxysmal Nocturnal Hemoglobinuria, etc.
    • ITP
    • Sepsis
    • SLE
    • Viral infections (HIV, mumps, varicella, EBVS)
  • Management
    • Consult Hematology!
    • AVOID Platelet Transfusion if possible!
      • It can lead to renal failure, higher rates of arterial thrombosis and death
      • Should be AVOIDED EXCEPT in life-threatening bleeding or ICH
    • Plasma Exchange (Plasmapheresis) is First Line treatment!
      • Replaces defective or insufficient ADAMTS-13 and clears vWF multimers
      • LDH can be used to evaluate for treatment response
    • FFP Transfusion
      • Contains ADAMTS-13
      • Can be helpful if delay in plasmapheresis
    • Transfusion of RBCs (indicated ONLY in severe bleeding with a delay in plasma exchange)
    • Glucocorticoids
      • Adjunct Treatment and do not replace plasmapheresis
      • 1mg/kg Prednisone PO or Solu-Medrol 125mg IV
    • IVIG
      • Not first line but may be used in those who fail plasmapheresis
    •  Splenectomy
      • Last line therapy after stabilization
      • Inhibitor antibody is made in the spleen

Suspect TTP in any patient with MAHA and thrombocytopenia!

Case presented by Dr. Yenisleidy Paez Perez, DO

ACEP Now Review on LVADs

Check out this excellent review on managing patients with LVADs from this month’s ACEP Now publication which was written by our own Dr. Yenisleidy Paez Perez, DO PGY-3 and one of our newly graduated residents, Dr. Terrance McGovern, DO. The article is entitled ‘How to Manage Emergency Department Patients with Left Ventricular Assist Devices.” Click the link below to be forwarded to the article.

http://www.acepnow.com/article/manage-emergency-department-patients-left-ventricular-assist-devices/

TLC: Triple Lumen Complications

Placing central venous cathethers, whether under ultrasound guidance or based off of your landmarks can be difficult and still prone to many complications.  With the increased use and now standard of care for placing central lines with ultrasound guidance you would think we are immune to the “catastrophic” complication of an inadvertent arterial cannulation.  But does ultrasound make us infalliable? Are there other methods that we can use to confirm venous placement of these large catheters?

Traditionally, we have looked at the color and pulsatility of blood coming from the needle hub before placement of the guidewire, but as you can imagine this is known to not be the most reliable; most of us aren’t going to go through the hassle of checking a blood gas off that blood either.

Troianos et al. found that ultrasound guidance reduced the incidence of arterial puncture from 8.4% down to 1.4% during attempted IJV cannulation.  That’s great that it decreased the incidence, but when looking at the complications such as airway obstruction, hemothorax, pseudoaneurysms, AV fistulas and stroke, 1.4% is not something to sneeze at.  So, keep in mind that although it does reduce the frequency of arterial puncture, it does not eliminate it entirely!

Despite the use of dynamic ultrasound guidance, there are still numerous reports of arterial placement of large bore catheters due to a couple reasons: 1. The needle tip may not be seen in the same plane of the ultrasound and confused with the shaft of the needle.  2. The needle may be in the vein, but the needle may move into the artery during placement of the guidewire after most of us have abandoned the ultrasound visualization.  Ideally, after the guidewire is placed we should make it a habit to confirm the guidewire is in the vein before dilating the vessel.

Management of Arterial Cannulation

Despite our best efforts and even the most astute ultrasonographer there is always the potential for an inadvertent arterial cannulation, but what do we do once we have figured that out?

Option 1: Just old fashioned PULL AND PRESSURE: essentially this is exactly as it sounds. You pull out the catheter and apply pressure, just like any other line that is being removed. This is probably most reasonable for femoral artery cannulations, but there still remains a possibility of false aneurysms and AVF as late as 2 weeks after removal with the pull and pressure technique.  Pull and pressure isn’t supposed to be used for carotid or subclavian arterial cannulations.  One convincing piece of evidence is that there is an immediate stroke risk of 5.6% after removing carotid cannulations with this technique.  Of 11,874 internal jugular vein cannulations, 20 ended up being carotid artery cannulations.  19 of these 20 were removed using the pull and pressure technique; six patients suffered complications and two of the patients died.

Option 2: Surgical ENDOVASCULAR repair:  The more preferable method, especially for removal of carotid and subclavian arterial cannulations, is to involve our vascular surgeon colleagues.  Just leave the line secured to the neck and get them involved. Some are going to request a formal ultrasound of the carotid or even sometimes a CT angio of the neck to check for extravasation, pseudoaneurysms, AVF and the location of the catheter.

Key points to remember

  1. Arterial cannulation can occur despite use of ultrasound guidance
  2. The American Society of Anesthesiologit’s guideline for CVC placement states that color and pulsatility are NOT reliable for distinguishing vein from artery.
  3. The pull/pressure technique is associated with significant risk of hematoma, airway obstruction, stroke, and false aneurysm especially when the site of arterial trauma cannot be effectively compressed
  4. Low IJV placement can injure the subclavian or innominate arteries
  5. Endovascular treatment is safe for management of arterial injuries that are difficult to expose surgically, such as those below or behind the clavicle.
  6. Normal Carotid Duplex after removal of a catheter form carotid artery does NOT rule out the possibility of a stroke
  7. False aneurysms or AV fistulae can occur LATE, up to 2 weeks after the “pull and pressure” technique so close follow up is needed

Post by: Dr. Yenis Paez-Perez, DO

 

 

Blunt chest trauma

Being in even the most benign car accident imaginable, can be stressful for patients.  Inherently, if they have any chest pain they’re going to be convinced that they’ve sheared their aorta right off its hinges.  While that may be of concern to them, we are pretty certain that their aorta is still intact if they still are alive, but did they sustain a cardiac contusion? How do we figure out if they had one?  And what the heck do we do with them if they did in fact have a cardiac contusion?

1) What are we concerned about in blunt chest trauma?
There are many clinically significant injuries possible in the setting of blunt chest trauma. One that comes to mind is the nebulus diagnosis of “cardiac contusion.”  A lot of the controversy and uncertainty comes from the unclear definition of cardiac contusion which seems to encompass things like myocardial rupture, valvular injury, arrhythmias, cardiac dysfunction, etc. In my mind these types of patients would be more clinically apparent so we’ll focus on the patients who may appear well or relatively so.

2) Do we need to get a troponin in blunt chest trauma?
The answer is yes and no. There is a “guideline” answer and a practical one.
The guideline answer is yes. The 2012 EAST practice guideline for blunt trauma recommends BOTH an EKG and troponin. They state based on their references that a normal EKG in blunt chest trauma has a NPV of 95%. This increases to 100% with a normal troponin. There are several studies that support the use of troponin in this setting and there are instances when EKGs may be normal with a positive troponin. One recent study showed a troponin at 24 hours had 100% NPV for severe cardiac injury.
But the practical answer may be no. There are other studies that are less optimistic regarding the sensitivity and specificity and discourage the use of troponin as a gold standard for diagnosing cardiac contusion from blunt trauma. Another study showed that positive troponins were not a strong predictor of abnormalities on echocardiogram. So getting a troponin may not even matter. However other studies suggested that a positive troponin may be indicative of cardiac contusion or underlying cardiac issue, which brings us to our next question.

3) What do we do with a positive troponin in blunt chest trauma?
One of the arguments against getting a troponin is not knowing what to do with it. If it is negative can they go home? If it’s positive do they need to stay? A 2013 prospective study out of Iran does not recommend troponin as a gold standard in cardiac injury but does encourage intensive cardiac monitoring if an elevated troponin is found. Another study showed that elevated troponin was linked to arrythmias during the patients stay.  So this would suggest admission and tele monitoring for a patient that may have otherwise gone home.

4) Does this change the patients outcome?
Probably not. Three older studies looked at outcomes of patients with cardiac contusions and they really have no long term sequelae and do well.

What’s the bottom line?
Being in a trauma center I would follow the trauma guidelines of getting both an EKG and troponin in the setting of blunt chest trauma. If this is negative with a negative EKG and the patient appears well clinically then likely discharge. However if they have an isolated positive troponin then I would consider admission for 24 hour monitoring for arrythmias with a consideration for inpatient echocardiogram with a reassuring knowledge that they will almost absolutely do well long term.

Post by: Dr. Jordan Jeong, DO (@jeongjom)

Time for Terlipressin?

Correct, we don’t have terlipressin in the US, yet… Hopefully, sometime in the not so far off future we’ll have the chance to play around with it. Essentially it’s a synthetic analog of vasopressin which we are more familiar with. There’s some written about its use in variceal bleeds and here is a cool little study from Egypt using it for refractory septic shock.

They enrolled 80 ICU patients that were in refractory septic shock; meaning that they had to meet sepsis criteria and have the following three criteria:

  1. SBP < 90mm Hg or MAP < 70
  2. Received at least 1000ml of IVF or CVP 8-12cmH2O
  3. Necessitated more than 0.5 mcg/kg/min of norepinephrine

The 80 adult patients were split into two, pretty well matched groups, of 40. One group received adrenaline (0.2ug/kg/min) as their second-line vasopressor and the other group received a continuous infusion of terlipressin (1.3ug/kg/hr). This study was interesting because it only lasted for the next 6 hours after the second vasopressor was started. Unfortunately, they really didn’t look at patient related outcomes, but instead their primary endpoints were:

  1. MAP > 65 mmHg
  2. Systemic vascular resistance index > 1300 dynes s/cm5/m2
  3. Cardiac index > 4 L/min/m2
  4. Oxygen delivery index (DO2I) > 550 ml/min/m2

From an Emergency Medicine point-of-view the MAP is probably what we are most familiar with and is an easy enough measure to monitor in the ED.  After initially starting with a statistically equivalent MAP before the start of the second vasopressor, to having a statistically significant difference (p<0.001) after the 6 hours is hard to ignore despite the lack of reported clinical outcomes. This was in addition to showing improved hemodynamic measures and decreased doses of norepinephrine needed in the terlipressin group. This by no means is the do-all and end-all for terlipressin, and doesn’t mean we start throwing it at everything with hypotension when it gets approved in the US. Might as well get familiar with it now though, so when it does show up there are no surprises.

Post by: Terrance McGovern DO, MPH (@drtmcg13)

Stressed vs unstressed volume

Dr. Rory Spiegel, from EMNerd, wrote a recent piece in Clinical and Experimental Emergency Medicine about how our undying love for left ventricular function in shock patients is perhaps overdoing it and the focus should rather be on the venous return. In the 1950’s Guyton et al described the three factors that affect venous return: 1. Right atrial pressure 2. Mean systemic pressure (Pms) 3. Vascular resistance.

The Pms is something that we don’t refer to often in critical care, but as Spiegel argues, should receive more respect than it does. In simple terms, Pms provides the pressure needed to produce a gradient from the venous return into the right atrium for forward flow. Spiegel provides a great analogy using a bathtub and bucket model to explain the physiology, but I’m going to attempt another analogy using a water balloon.

The Pms is composed of the blood within the venous system and the pressure exerted by the vascular bed. In the water balloon analogy, the water within the balloon is the venous blood volume and the physical balloon is the vascular bed. You can imagine, there is a certain amount of water that a water balloon can hold before the balloon starts to expand and enlarge, this is the unstressed volume. As you fill the balloon it grows and the pressure exerted by the walls of the balloon increases, this is called the stressed volume. The stressed volume produces increased Pms and subsequently increases venous return to the right atrium. Now, think of a septic shock patient as an old, ratty balloon that has been inflated too many times and has lost of lot of its elasticity. The amount of water needed in these septic balloons to get to a stressed volume is much more than a normal, healthy, brand-new balloon. Hence why we start with multiple liters of fluid resuscitation in septic shock patients, to try to get them to a stressed volume and improve the venous return. When this doesn’t work, we move onto vasopressors to clamp down on the vascular bed (squeeze the balloon) as another means of increasing Pms and venous return.

With summer around the corner, it’s going to be hard to ignore the similarities between helping your kid prepare for their next water balloon battle and dumping 30cc/kg of fluid into that old ratty, septic water balloon. Check out Spiegel’s piece in Clinical and Experimental Emergency Medicine for great review of mean systemic pressure and its relation to stressed and unstressed volume here.

Post by: Terrance McGovern DO, MPH (@drtmcg13)