Hemorrhagic shock secondary to GI bleed with recent PCI for NSTEMI on DAPT… Did I mention severe aortic stenosis as well? How about all of these in one patient at the same time? 11/29/2018

Narges presented a very complicated patient, who presents with 2 days of abdominal pain and melena. He had a PCI 4 days prior with a drug-eluting stent deployed at the LAD, and he was discharged on aspirin and ticagrelor (PLATO trial, superior to clopidogrel). On presentation he was in hemorrhagic shock, with notable hematochezia on exam, encephalopathy, and a 4/6 systolic murmur with carotid radiation which turned out to be an undiagnosed severe aortic stenosis.

To briefly summarize his main problem list:

  1. Hemorrhagic shock secondary to UGIB
  2. CAD with recent NSTEMI s/p DES to LAD x1 on DAPT
  3. Severe aortic stenosis, newly diagnosed

Question is, what to do if you see a patient like this? Let’s break it down.


 

Antiplatelet and PCI

  • Drug eluting stents (DES) are designed to have lower rates of late re-stenosis than bare metal stents (BMS), but they are at higher risk for in-stent thrombosis due to delayed endothelialization.
  • Some terminology:
    • Stent re-stenosis:
      • Gradual narrowing of the stent segment, usually occurs 3-12 months after stent placement.
      • Can present as recurrent angina vs full blown MI
    • Stent thrombosis
      • Abrupt thrombotic occlusion of a previously patent stent, usually catastrophic MI
  • Duration of DAPT? It depends! Per the 2016 ACC/AHA guidelineDAPT.png

In a nut shell:

Elective PCI in stable CAD:

  • BMS: At least 1 month of DAPT
  • DES: At least 6 months of DAPT

Exact duration is yet to be determined; there is some evidence of decreased stent restenosis (DAPT trial) with longer duration of DAPT but at the expense of all cause mortality and bleeding complications. There are also newer studies (i.e. ARCTIC Interruption) that found no benefits with longer duration of DAPT.

For PCI in setting of ACS, however, the guideline is different:

Anti-platelet duration in setting of ACS

  • Medical Therapy: At least 12 months of DAPT
  • PCI (BMS or DES, doens’t matter): At least 12 months of DAPT
  • CABG: Also at least 12 months of DAPT

In patients with high bleeding risk or personal history of bleeding and/or long term NSAID use, preemptive prophylaxis with a PPI can be considered. If bleeding risk is significant, you can potentially decrease DAPT duration to at least 6 months, on a case-to-case basis.

Now keep in mind our patient has a DES deployed 4 days ago and he’s now bleeding…


GI Bleed

Risk Factors

  • Alcohol
  • NSAID
  • Anticoagulation
  • Cirrhosis
  • Cancer

Presentation

  • UGIB: BUN/Cr ratio > 30 usually (not sensitive but specific), melena (gut transit of blood)
  • LGIB: bright red hematochezia, lower BUN/Cr ratio, but do not be fooled, can be seen in brisk UGIB (especially in this patient).

Management

  • Airway protection
  • Large bore IVs (18 G), Cordis, IO (they work wonders in a pinch!)
  • Fluid resuscitation
  • Anti-acid (i.e. Protonix)
  • Octreotide if suspecting variceal bleed, if catastrophic variceal bleed, consider deployment of a Blakemore/Minnesota tube
  • Antibiotics for primary SBP prophylaxis if cirrhotic
  • Blood product administration
  • GI consultation, urgency depending on clinical status, EGD

High risk features on Endoscopy

The patient underwent EGD and a duodenal ulcer that was actively bleeding was found. There are certain features of an ulcer that we can use to risk stratify and determine how likely intervention will be successful, and how likely the ulcer will rebleed. This is the Forrest Classification, first published in the Lancet in 1974. Our patient in this case is class 1B, and he ended by rebleeding twice requiring additional endoscopic intervention.

Picture1

Source: Alzoubaidi DLovat LBHaidry R. Management of non-variceal upper gastrointestinal bleeding: where are we in 2018? 

Failure of endoscopic therapy

  • Predictors: active bleeding at time of endoscopy, visible vessel, > 2cm, posterior duodenal ulcers, and gastric ulcers on the lesser curvature are associated with higher risk of treatment failure/rebleeding.
  • First line: 2nd endoscopic intervention
  • If recurrent bleeding persists, surgical options or IR embolization should be considered

The key question here is, when to resume DAPT? The decision will have to be individualized and most would recommend restarting ASAP as soon as patient is clinically stable… At the same time, pt has one other newly diagnosed problem that makes his management tricky…


aorticvalvearea-classification-aorticstenosis-meangradient-cardiology-original

Source: grepmed

Severe Aortic Stenosis

Criteria:

  1. Area < 1cm2
  2. Mean trans valvular gradient > 40 mmHg
  3. Peak velocity > 4m/s

Referral to Cardiology because it is actually more complicated than this, there is also pseudo severe where AVR is not recommended, Low flow AS, low gradient AS, or both LF LG AS.

  • Pseudo-severe: mild to moderate AS, low gradient, underlying myocardial dysfunction leading to poor valve opening. No benefit in AVR
  • LF LG AS:
    • AVA < 1cm2, but gradient < 35mmHg
    • Must distinguish from pseudo severe AS. Do dobutamine stress echo
      • If AVA remains the same, gradient inc, confirms true severe AS
      • If AVA improves while mean gradient remains the same, this is pseudo-severe AS, manage medically.

Epidemiology

  • < 70: Suspect bicuspid aortic valve
  • > 70: Progressive valvular fibrosis/calcification
  • Developing country: Rheumatic fever

Pathophysiology

  • Over time leads to LV hypertrophy (concentric), muscle hypertrophy. Leads to heart failure over time.

Presentation

  • Asx
  • Sx: SAD syncope, angina, dyspnea

Management

  • TAVR (transcatheter) vs SAVR (surgical), TAVR is non-inferior (PARTNER A, PARTNER B, SURTAVI trials) but has other complications to consider,
  • Can think about the transcatheter approach in high surgical risk patients.

In setting of hypotension

  • Patients with critical AS are highly preload dependent:
  • Cardiac Output (CO) = Heart Rate (HR) x Stroke Volume (SV). In patients with severe AS, CO is fixed due to physiologic limitations of a small outlet.
    • Increasing HR can help with CO but you run the risk of increasing myocardial O2 demands…
    • Also in terms of volume, pts with severe AS usually has a degree of diastolic dysfunction (decreased compliance due to a hypertrophied ventricle). As you can imagine, if you push too much fluids into a non-compliant system, back up can occur leading to pulmonary edema thus respiratory failure…
  • Choice Pressors: no absolute contraindication to any but phenylephrine has been suggested in some anesthesia text books as first line
    • Rationale: Pure alpha, increases DBP (diastolic blood pressure), which in turns inc coronary perfusion pressure (CPP = DP – PCWP (LVEDP))
    • Won’t induce tachycardia (if anything induces a mild reflexive bradycardia which decreases myocardial O2 demands).
    • Epi has been associated with higher incidences of arrhythmias

Hypothermia and Myxedema Coma – 11/13/18

Thanks to Austin for presenting the case of an elderly woman with h/o psychiatric disorder who presented with acute/subacute onset of AMS, severe hypothermia, sinus bradycardia, and hypotension with work up revealing hypothyroidism suspicious for myxedema coma!


Clinical Pearls

  • Exam findings for hypothermia change depending on severity of hypothermia (see below).
  • It is crucial to measure core body temperature for accuracy especially when you are rewarming the patient (esophageal is the best, rectal/bladder are ok prior to rewarming but can remain low in spite of increasing core body temp so do not rely on these metrics alone)
  • Think of etiologies of hypothermia broadly within the categories of increased loss or decreased heat generation.
  • The most common causes of hypothermia are sepsis, exposure, and hypoglycemia.
  • The hallmarks of myxedema coma are AMS, hypothermia, and a precipitating event (i.e. infection, exposure, meds, etc.)
  • Myxedema coma is a medical emergency with a high mortality rate.  So consult endocrine early when you are suspecting it.
  • Always treat myxedema coma with levothyroxine AND steroids until you have ruled out a concurrent adrenal insufficiency.

HYPOTHERMIA

Types:

  • Mild (32-35°C)
    • Clinical manifestations
      • Shivering, rigors
      • ↑ HR, ↑ RR, ↑ BP, hyperventilation
      • Cold diuresis
        • Body’s attempt to preserve heat.  When peripheral vasoconstriction occurs to keep blood closer to vital organs, BP rises.  Kidneys see this rise in BP and act to correct it by dumping fluid! (Oh kidneys…)
    • Treatment
      • Passive, external
        • Blankets
        • Humidified inspired air
  • Moderate (28-32°C)
    • Clinical manifestations
      • ↓ shivering
      • Confusion, slurred speech
      • ↓ HR, hypoventilation
      • Can also start to notice other cardiac manifestations such as prolonged QTc, QRS, osborn (J) waves, ST elevations/depressions.
      • ↓ renal blood flow
    • Treatment
      • Passive, external (see above) PLUS
      • Active external
        • Forced heated air
        • Warm blankets
        • Warm water immersion
      • Active internal
        • Warm humidified air (42°C)
        • Warm IV fluids (42°C)
        • Body cavity lavage (in trauma patients only)
  • Severe (<28°C)
    • Clinical manifestations
      • NO shivering
      • Edema (due to poor renal blood flow) of extremities and lung
      • ↓ HR, ↓ BP (due to drop in cardiac output), hypoventilation, ventricular arrhythmias
      • Cardiac manifestations more common as with moderate hypothermia
      • AMS
      • Paradoxical undressing
        • mechanism is poorly understood but thought to be due to paralysis of the nerves regular vascular muscle tone leading to vasodilation and sensation of a heat flush which results in the patient wanting to take their clothes off.
    •  Treatment
      • Any of the above (passive external, active external, active internal) and/or
      • Extracorporeal
        • HD
        • ECMO

Etiologies of hypothermia:

Capture

Items in red above are the most common causes of hypothermia.

Lab findings:

  • Less reliable since labs have to be warmed prior to processing
    • ABG is often inaccurate
    • Coagulopathy may be masked
    • Hyperkalemia due to rewarming

Complications of rewarming:

  • Hypotension due to peripheral vasodilation
  • Ileus and urinary retention
  • Worsening coagulopathy
  • Arrhythmias
  • Hyperkalemia
  • Core temperature after-drop (a condition in which cold peripheral blood gets shunted to the core and results in further decline in temperature.  You can avoid this by active internal rewarming like warmed IV fluids)

MYXEDEMA COMA 

Learn all about it from our prior blog post here.

Metformin Associated Lactic Acidosis (MALA) 9/17/2018

Thanks to doctor-in-training Emma who presented a case of an elderly woman, on dialysis, who came in with SEVERE lactic acidosis due to a variety of factors, but largely contributed by being prescribed metformin 2 weeks prior to presentation.

We will use this case to illustrate several concepts:

On initial presentation, pt was in a state of shock. If you remember from medical school, there are mainly 4 types:

  • Cardiogenic
    • Myopathic (DCM, acute MI)
    • Mechanical (Acute MR, VSD, severe AS)
    • Arrhythmia
  • Hypovolemic
    • Hemorrhage, volume depletion
  • Distributive
    • Sepsis
    • Anaphylaxis
    • Neurogenic (spinal cord injury)
    • Endocrine (myxedema, Addison’s)
  • Obstructive
    • Pericardial tamponade
    • PE
    • Pneumothorax

Shock can also be approached from a cardiac output standpoint to help differentiate the potential causes:

Capture

If someone is hypovolemic, but he/she is found to be hypotensive but bradycardic (instead of tachycardic), remember from physiology:

MAP = CO x SVR, where CO is cardiac output, SVR is systemic vascular resistance

CO = SV x HR, SV is stroke volume, and HR is heart rate.

Hence in a state of hypovolemia, the body will attempt to maximize CO by increasing HR to maintain adequate MAP. If you see the opposite though, there could be something else going on…

  • Cardiac: MI, conduction abnormalities, infectious (Lyme, Charga’s)
  • Toxic/Meds: CCB, Beta blocker, Dig, Alpha 2, organophosphate
  • Lytes: Hyperkalemia -> heart block -> sinus arrest
  • Endocrine: Hypothyroidism (myxema coma), adrenal insufficiency
  • Environmental: Hypothermia
  • Neurogenic shock

 

Acid-Base: Acid-base disorders can appear daunting, but the following algorithm can make things simpler if followed consistently. We will work through this patient’s acid/base disorder together. Her HCO3 is 6, AG of 52, with an ABG of 6.83/13/170.

  1. Look at the pH: < 7.4 automatically means some sort of acidosis is going on.
  2. Next look at the PCO2, if it is in the same direction as the pH (low PCO2 in this case, and low pH), then it is suggestive of a primary metabolic rather than a respiratory issue causing the acidosis. If pH is low and PCO2 is high, then there is high suspicions for a respiratory process driving the acidosis.
  3. Look at the Anion Gap, which in this case in 52. Go through your differential for AGMA.
  4. Calculate the Delta Gap. This basically is a way to assess whether a mix acid/base disorder exists after taking into account the AG. To help illustrate:Capture2
  5. Delta gap = calculated AG – normal AG = 52 – 12 = 40. Now there are several ways to do this, but one method that’s quick and simple is to simply add this delta gap to the measured bicarb and see what other metabolic acid/base disorders can be hiding beneath the anion gap. In this case, 40 + 6 = 46, which is suggestive of an underlying metabolic alkalosis.
  6. Lastly, calculate compensation. For AGMA, use Winter’s Formula = 1.5 (HCO3) + 8 +/-2. The calculated PCO2 should be 15-19. Since our measured PCO2 is 13, which is lower than expected, then this is suggestive of an underlying respiratory alkalosis as well, probably due to sepsis.
  7. Our final answer for the acid/base disorder for this patient is: AGMA with metabolic alkalosis and concurrent respiratory alkalosis!

 

Lactic Acidosis: Traditionally we view this as a sign of sepsis, or a marker of tissue hypoperfusion. However this is not always the case!

  • Type A: Inadequate oxygen delivery
    • Rule of thumb: Tissue hypoperfusion, tissue ischemia
    • Can also be seen with increased anaerobic muscular activity, like generalized convulsions in a seizure
    • Can also be seen in hypoxemia, severe anemia
    • Cryptic shock (elevated lactate, okay BP), similar to overt septic shock in terms of mortality in setting of severe sepsis.
  • Type B: altered physiology, others
    • B1: Underlying disease, malignancy, hepatic & renal failure
    • B2: Drugs, toxins
    • B3: Inborn errors of metabolism, enzyme deficiency
  • Management: Tx the underlying cause, bicarb controversial, studies have shown no benefits? But most experts would agree with usage in critically ill patients with profound acidemia.

 

MALA: Lastly, this case illustrates the dangers of metformin, in the right setting, can lead to severe acid/base disturbance (MALA).

  • Do NOT use metformin if GFR < 30, be careful in CKD patients.
  • If suspecting metformin toxicity and pt is hyperglycemic, this is a sign of severe toxicity.
  • Always do a thorough med reconciliation on every single patient!