Shock or not shock, that is the question

Standard chief complaint - 8o-something guy sent from dialysis for a fever.  He had just had a graft put in his arm a couple of weeks prior, but he also had a tunneled IJ catheter and several other potential sources for his fever.  The patient denied any symptoms other than a productive cough and shortness of breath that he said was chronic and unchanged, however when his significant other arrived, she said that the cough and shortness of breath were new and worsening over the previous week, and that he also seemed a little confused over the last couple of days.

The patient was febrile, mildly tachypneic, tachycardic, and hypoxic, with an initial blood pressure 160s/70s.  He was A&Ox4.  Antipyretics were given, and the work-up was started.  He didn't look overly toxic or in any distress.  His fever resolved, HR returned to normal, and RR decreased to approximately 20.  His initial lactate was 2.5.

What I want to reflect on in this case is the blood pressure.  As the remainder of his vitals improved, his BP started to trend down, to SBPs of 100s, then 90s, 80s, then one in the 70s.  I attributed the initial drop in BP due to resolution of his fever, but when it got into the 80s, I started to give him small fluid boluses totaling about 500 cc, plus he was getting antibiotics, and being that he was a dialysis patient, I wanted to go slow.  His mental status never changed during this period of hypotension, and his HR stayed right around 100.  His next couple of pressures were back in the 90s and 100s.  Appropriate surgery and medicine consults were called, and he was signed out to the step down unit for admission.  Subsequently a STEMI came in, so I was pulled away for about 20 minutes, and when I went back to the room the MICU resident was there and the patient had been started on dopamine.  Apparently his SBP dropped back down, as low as 60s.

I've heard multiple lecturers and ED attendings say that Emergency Physicians aren't really good at recognizing shock.  I'm not quite sure why this is, but I can postulate a couple of reasons.  First, we see a broad range of vitals in a lot of different people, and maybe we just don't react to vital signs like we should.  SBPs >200 in Philly are a dime a dozen, as are blood sugars >400.  We also have ESRD patients that always run low after dialysis, and this patient had just been dialyzed.  Second, I think that suspicion of shock is often based on the clinical appearance of the patent.  This guy was awake, oriented, and without real complaint, looked well perfused, wasn't overly tachycardic, and I didn't really feel that he was in shock.  His lactate was right on the cusp of abnormal, but he didn't look toxic.

I think that had I recognized that this patient was in septic shock earlier, and not just hypovolemic from dialysis, more aggressive initial fluid resuscitation may have been able to save this patient a central line, dopamine drip, and short MICU stay. The patient's BP improved with the dopamine and continued fluid resuscitation, and his mental status seemed to improve to better than when he had initially arrived with a hypertension.  He ended up only being on the drip for a few hours and doing just fine, but still a good case for reflection.

GI Bleed? Occam vs Hickam

The other night a patient came in from a nursing home by EMS, reportedly unresponsive with respiratory with agonal breathing.  He had been intubated en route by paramedics.  Paperwork from the nursing home said Hep C, cirrhosis, and end stage metastatic liver cancer.  There appeared to be coffee ground emesis on his face and linens, and when asked, paramedics stated that he vomited on their initial intubation attempt.  He was hypotensive and unresponsive (HR was 90s, which was surprising since he wasn't on any rate reducing medications).  His rectal temp was 34.9.  An NG tube was placed which drained 500cc of dark blood/coffee ground stomach contents.  This was a GI bleed, and all the appropriate steps were initiated. Things were somewhat delayed as he had no vascular access (EMS had placed an IO that wasn't flowing), and we were unable to get a pulse ox or cardiac monitor to read on the patient even after switching out monitors several times.  Central access was obtained, and he received 2L NS rapidly, and 2 units of unmatched blood were ordered.  The blood and additional fluids were given through the Ranger.  GI and MICU were contacted.  A CC lytes (point of care VBG) returned with a pH <6.91, lactate >139, K 8.3, and, surprisingly, a HCT of 38.

This is where the the thought process changed.  This patient had a GI bleed, but is that what was causing his hypotension, altered mental status and hypothermia?  Our job as emergency medicine physicians is not to observe the way that something walks, and the way it quacks, then to say it's a duck.  Our job is to say this may be a duck, or a goose, or a swan, etc... and in critical patients, to provide both diagnostic and therapeutic interventions at the same time.  

Now this normal Hct could have been due to hemoconcentration or lag in a Hct that has yet to drop.  However this patient has the right to have as many medical problems as he damn well pleases.  Maybe the bleeding resulted from the acidosis and hypothermia from an already established sepsis.  Liver patients are obviously prone to sepsis from multiple sources, and his CXR showed bilateral opacities concerning for aspiration vs pneumonia.  The patient was also on Dexamethasone for his bone mets - is he adrenally suppressed?  Myxedema coma is also on the differential.  Was the hypothermia environmental?  The nursing home reported that his symptoms had only started 15 minutes prior to arrival, but maybe that is just when they noticed it.  He could have been uncovered, cold, and slowly deteriorating over the course of the day.  

In reality it was probably multifactoral.  This guy was really sick, and his family decided to withdraw care while he was in the ED.  It was a good case to remind me not to anchor on the first and "most obvious" diagnosis.

Suicidal in a cemetery

It's 7 am, the pod is just opening, and EMS brings me my first patient of the shift.  30s, male, suicidal, found in a cemetery with a self inflicted arm laceration in the antecubital fossa.  He also admits to taking four Oxycontin 15 mg pills about four hours prior.  The patient is drowsy but arousable and oriented, and complaining of nonspecific lower abdominal pain.  The arm bandage is bloody but not soaking through, and when removed, there is no active bleeding.  EMS was unsure of how much blood he had lost in the field.  All the usual stuff is done.  Initial vitals show patient with a HR of 130s, BP 97/40, normal respiratory rate.  His clothes are wet, and he is cold to the touch, but has a normal oral temperature.   EKG w/ sinus tachy, nl QTc, nl QRS.  Physical exam is remarkable only for the laceration and diffuse lower abdominal tenderness without guarding or peritoneal signs.  There were no signs of any toxidrome.

Seems pretty straight forward - supportive treatment, end-tidal CO2 monitor to monitor for respiratory depression from the opioid use, basic labs, check tylenol/aspirin level, IV fluids, laceration repair, make sure vitals normalize, and ship to the crisis response center for psych eval.

He had been in the department for approx 10 minutes when his his blood pressure started to drop - SBP 80s, then 70s.  A second line was obtained, IVF opened wide, and 2 units un-crossed blood was ordered.  His point of care VBG had a Hct of 32 and a lactate of 83.  A FAST exam was started, as he had the abdominal pain, with no fluid seen in the RUQ or suprapubic areas.  During the FAST, the new bandage that was placed on his arm became blood soaked and started dripping on the floor.  On re-exploration, there was a partial laceration of the cephalic vein that had started to bleed profusely.  A normal IV tourniquet was applied just below the laceration, and the vein was isolated and tied off with nylon suture.  Due to the wound and hypotension, the patient was moved to the trauma bay for eval by the trauma team.  His heart rate and blood pressure responded to 2 units of blood and 3 L NS.  His mental status remained unchanged throughout the event.

This patient had several signs of hypovolemia, including altered mental status, tachycardia, some degree of hypotension, with cutaneous vasoconstriction.   I think the chief complaint of suicidal ideation and initial assessment of the laceration led me to attribute these clues to a possible unreported ingestion or environmental exposure, not to his wound and acute blood loss.  It wasn't until his blood pressure started to drop that I realized he could have had significant blood loss in the field and needed to be aggressively resuscitated.  This was not confirmed, but the abdominal pain may have been due to gut ischemia from hypoperfusion.  Interestingly, he had multiple acute splenic infarcts on his abdominal CT.

Intro

My name is Aaron, and I'm currently an emergency medicine resident at Einstein Medical Center in Philadelphia.  I'm sure just like every other physician, I have cases that I can't help but mull over in my mind for several days, considering the details of my approach and decision making, and how I could have done things different or seen certain clues sooner - kind of a Monday morning quarterback self assessment.  I'm a big fan of FOAM (Free Open Access Meducation), so I figured I'd start blogging the case, how it presented, how the case was handled, and my "Monday morning" thoughts, both as a reference for myself and to put it out there for anyone else who is interested.  Any comments are welcome, as I'd like this to be as educational as possible.  We'll see how it goes.