Status Epilepticus & Serotonin Syndrome

Today we talked about the case of a young woman who presented after suicide attempt by ingestion of multiple prescription medications, found to be obtunded, initially in status epilepticus and later with exam findings concerning for serotonin syndrome.


Clinical Pearls

  • Continuous EEG is indicated if a patient is not returning to baseline mentation 15 mins after a seizure to rule out non-convulsive status epilepticus.
  • Status epilepticus is defined as a seizure lasting > 5 mins or > 2 discrete seizures between which there is incomplete recovery of consciousness.
  • Treatment of status epilepticus involves acute management with IV/IM benzos, urgent long-term control with IV fosphenytoin (preferred), phenytoin, or valproic acid.  Remember that keppra is more useful in suppressing future seizures than treating an acute episode.
  • Serotonin syndrome is a clinical diagnosis and manifests with neuromuscular activation like tremors, hyperreflexia, and clonus (generally worse in lower extremities).  Use Hunter’s criteria to help with diagnosis.

Status Epilepticus

  • When is continuous EEG needed?
    • If patient is not returning toward baseline in 15 mins after a seizure, goal is to rule out nonconvulsive seizures
  • How to define status?
    • > 5 mins OR
    • > 2 discrete seizures between which there is incomplete recovery of consciousness
  • Non-convulsive status epilepticus
    • Suspect if LOC not improving by 10 mins after cessation of movement
    • Mental status remains abnormal for 30-60 mins after movement cessation
    • Dx requires a 24-hour EEG (we don’t have one ☹)
    • Treatment is the same as generalized status epilepticus, but prognosis is worse (mortality 65% vs 27%)
  • Treatment of status
    • Assessment and supportive treatment
    • Initial pharmacologic therapy
      • Ativan (2 mg IV q1-2 mins), total dose 0.1mg/kg
        • Watch out for respiratory depression and hypotension
        • Alternatives: versed 0.2mg/kg IM, valium 0.2mg/kg IV
    • Urgent long-term control
      • Fosphenytoin (preferred): 20 mg/kg at 150mg/min
        • Give extra 10 mg/kg if not responding
        • Dephosphorylates into phenytoin.  It’s more soluble in water and less likely to precipitate in the skin and vessels.
      • Phenytoin: 20mg/kg at 50mg/min (slower than fospheny)
        • If infused too fast, can irritate skin/vessels causing skin necrosis
      • Valproic acid: 20mg/kg at 5 mg/kg/min
        • Sometimes the preferred choice in patients with known generalized epilepsy b/c phenytoin can provoke absence seizures in that population.
      • What about Keppra?
        • Technically not FDA approved for status.  It has weak evidence to support its use.  More useful in suppressing subsequent seizures after status has been controlled.

Serotonin syndrome:

  • Clinical diagnosis. Serum serotonin concentrations do not correlate with clinical findings.
  • Severe disease can lead to DIC, rhabdo, renal failure, and ARDS.
  • Diagnostic criteria: use Hunter’s (84% sensitive, 97% specific)Hunter's decision rule
  • DDx
    • NMS
    • Anticholinergic toxicity
    • Malignant hyperthermia
    • Sympathomimetic intoxication
    • Sedative-hypnotic withdrawal
    • Meningitis
    • Encephalitis
  • Serotonin syndrome may be distinguished from other causes of agitated delirium on the basis of neuromuscular findings. Whereas patients with serotonin syndrome show signs of neuromuscular activation (eg, tremor, hyperreflexia and clonus that are greater in the lower extremities, ocular clonus, and increased muscle tone), patients with sympathomimetic toxicity or infections of the central nervous system lack these findings.
  • Treatment
    • Supportive care and sedation
      • Chemical sedation preferred over physical restraint
    • Autonomic instability
      • High BP: esmolol or nitroprusside (Short acting). Avoid longer acting agents
      • Low BP: neo or epi. Avoid idirect agents like dopamine because they are converted to epi and norepi.  When monoamine oxidase is inhibited, epi and norepi production at the cellular level is not controlled and could lead to an exaggerated HD response.
    • Hyperthermia
      • No benefit to Tylenol b/c increase in body temp is due to increased muscular activity rather than alteration in the hypothalamic temperature setpoint.
      • If temp >41.1, then sedate, paralyze, intubate
    • Antidote: cyproheptadine
      • Histamine receptor antagonist. Also has weak anticholinergic activity
      • 12 mg loading dose, then 2 mg q2h until clinical response is seen.
      • Is sedating (good) and can also cause transient hypotension.

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Hyponatremia due to secondary adrenal insufficiency

Thanks to Jess for presenting the fascinating case of a middle-aged woman with family history of autoimmune disease who presented with acute onset of fatigue and abdominal pain, found to have vitiligo on exam.  Work up revealed hyponatremia due to a secondary adrenal insufficiency, pancytopenia, and panhypopituitarism possibly due to a yet to be diagnosed autoimmune disorder!


Clinical pearls

  • Remember that hyponatremia is a problem of water regulation that can be compounded by low solute intake.
  • Primary adrenal insufficiency is disorder at the level of the adrenal glands and manifests with low sodium and high serum potassium levels.
  • Secondary adrenal insufficiency is disorder at the level of the pituitary and manifests with low/normal sodium and normal potassium levels (because low cortisol leads to high ADH levels and hyponatremia).
    • Make sure to do work up to rule out panhypopituitarism.  Keep in mind that the most sensitive test for HPA access integrity is LH/FSH.
  • Tertiary adrenal insufficiency is disorder at the level of the hypothalamus and presents similarly to secondary AI.
  • Test for adrenal insufficiency with a cort-stim test and/or AM cortisol and ACTH levels.

Hyponatremia

Remember these three steps to working up hyponatremia:

  1. Is there a sodium problem? check serum osm
  2. Are the kidneys responding appropriately? check urine osm
  3. Is ADH revved up for a hemodynamic reason? check urine Na 

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Adrenal insufficiency

Adrenal insufficiency
Source: NIDDK.gov

Primary AI:

  • Failure of adrenal glands
  • Causes: Addison’s (most common in the US), infiltrative processes (TB, sarcoid), hemorrhage, toxins
  • Labs would show ↓Na and ↑potassium (b/c aldosterone is gone)

Secondary AI:

  • Failure of pituitary (low ACTH)
  • Causes: pituitary lesions, surgeries, TBI, drugs
  • Clinically may present with loss of other anterior pituitary hormones
  • Labs would show ↓Na (because low cortisol leads to high ADH levels) but normal potassium levels (b/c aldosterone is active)

Tertiary AI:

  • Failure of hypothalamus (low CRH)
  • Causes: more commonly iatrogenic (cessation of high dose glucocorticoid therapy without taper) or post surgical interventions.

Hypopituitarism

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Hypophysitis:

  • Inflammation of the pituitary
  • Four categories based on histologic findings:
    • Lymphocytic
      • Most common form
      • Seen in late pregnancy and post-partum period
      • Also associated with CTLA4 inhibitors like ipilimumab
    • Granulomatous
      • Idiopathic or secondary to GPA, sarcoid, TB
    • Plasmacytic (IgG4-related)
    • Xanthomatous (most rare)
  • Clinical presentation
    • Headache out of proportion to exam findings
    • Preferential decrease in ACTH and TSH ⇒ adrenal insufficiency and hypothyroidism
  • Prognosis:
    • Pituitary size eventually normalizes but pituitary loss of function is often permanent.

 

Angioedema and hyperkalemia management

Thanks to Audris for presenting the case of a middle-aged man with vasculopathy on ACEi who presented with angioedema requiring intubation!  We discussed the  diagnostic work up and management of angioedema as well as hyperkalemia!


Clinical Pearls

  • First order of business when suspecting angioedema is the ABCs!
  • Treat angioedema in the acute setting with H1 blockers and steroids, even if you are suspicious of a non-histaminergic pathway.
  • Always assess for concurrent anaphylaxis (hypotension or bronchospasm in addition to hives or angioedema).  If anaphylaxis is present, then treatment involves IM 0.3-0.5 mg of 1:1000 dilution epinephrine (1mg/mL), repeat every 20 minutes until symptoms resolve (max 3 doses)
  • If you have access to a functioning kidney, favor loop diuretics over cation exchange binders (i.e. kayexalate) to lower serum potassium!
  • Patiramer is much better tolerated than kayexalate and has a more favorable side effect profile.
  • Calcium gluconate has a role in the treatment of hyperkalemia when EKG changes are present. Give a dose and repeat the EKG.  If no improvement, repeat to a maximum of 3 doses until EKG has normalized.

Angioedema 

  • 3 pathophysiologic subtypes:
    • Mast cell/histamine mediated
      • Etiologies:
        • Allergic reactions: food/insect stings, latex, drugs. Can also be idiopathic. IgE type 1 hypersensitivity
        • Direct mast cell release: drugs (opiates, contrast). IgE is not involved.
        • ASA/NSAIDs: via IgE or direct mast cell release
        • Chronic urticaria w/w/o angioedema
      • S/sx affecting organ systems other than the skin? Suspicious for anaphylaxis ⇒ give epi
      • Treatment: H1 blockers, glucocorticoids. 
    • Bradykinin mediated
      • Inhibition of enzymes involved in the degradation of bradykinin, or deficiency/dysfunction of complement C1 inh
      • More prolonged time course, develops over 24-46 hours and resolves within 2-4 days
      • Relationship between trigger and onset of symptom is not as apparent
      • Not associated with other s/sx. More common to have abdominal pain due to bowel wall involvement.
      • Treatment: bradykinin pathway mediators (ecallantide, icatibant), C1 inhibitor concentrate, or plasma replacement.
    • Unknown mechanism
      • Idiopathic angioedema
      • Infections (in children)
      • CCBs
      • Other drugs: sirolimus, everolimus, amiodarone, metoprolol, risperidone, paroxetine, and etanercept, inhaled cocaine.
      • Herbal meds
      • Urticarial vasculitis
      • Hypereosinophilic syndrome and Gleich syndrome

 

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Hyperkalemia

Agents that reduce serum potassium via transient intracellular shift:

  • Insulin: give with D50 if normoglycemic to avoid hypoglycemia and be sure to check FSG hourly for 4 hours after to ensure no hypoglycemia develops
  • Albuterol (10-20 mg) nebs: this is significantly higher than the dose we give in COPD (2.5 mg) and is equal to ~8 treatments! So make sure to continue the nebs when the patient arrives on the floor from the ER if they are still hyperkalemic.
  • NaHCO3: best for management of chronic hyperkalemia in the outpatient setting.  In the acute management of hyperkalemia, alkalinization of serum with a large bicarb load can lead to a reduction in serum calcium levels.  Lower serum calcium can lead to more cardiac membrane instability and fatal arrhythmias!

Agents that eliminate potassium from the body:

  • Loop diuretics: first choice if a functioning kidney is available!
  • Cation exchange binders: preferred when kidneys are not available
    • Patiramer (available at VMC), much more tolerable than kayexalate and highly effective at lowering serum potassium.  Like kayexalate, it works over hours to days.
    • Sodium zirconium: similar to patiramer but not currently available
    • Kayexalate: not pleasant to take orally. Also carries with it the slight risk of colonic ischemia especially in post renal transplant patients and those with baseline colonic dysfunction (due to infection or inflammation).
  • Dialysis

Indication for using calcium gluconate: when EKG changes are noted.  Repeat doses (maximum 3) until EKG changes have resolved.

A Beriberi Nice Case of… Thiamine Deficiency (1/9/2019)

Adam presented a case of a 32yo woman with an extensive alcohol history presenting with seizure in setting of recent cessation of alcohol. Pt has also been complaining of weakness in her legs to the point she could no longer walk, worsening vision, and urinary incontinence for the past few months. Per her family, she only ate one meal a day and she was quite picky in terms of her diet.

She was treated for alcohol withdrawal and delirium tremems. When she was stabilized, her neurological exam was concerning for significant weakness in proximal and distal upper and lower extremities, paresthesia, dysmetria, and hyporeflexia.  An EMG was done which revealed peripheral polyneuropathy. This constellation of symptoms (alcohol, poor nutrition, polyneuropathy) is consistent with… Beriberi!


Thiamine deficiency

Epidemiology

  • Developing countries
  • Alcoholics
  • Extreme poverty
  • Displaced populations, refugees

Common Risk factors

  • Poor nutrition
  • Alcohol
  • Weight loss surgery
  • Long term TPN

Presentation of Thiamine Deficiency

  • Wet beriberi
    • Heart failure due to thiamine deficiency (high out heart failure)
    • Vasodilation, tachycardia, widened pulse pressure, diaphoresis, lactic acidosis, peripheral edema
  • Dry beriberi
    • Peripheral polyneuropathy, affects predominantly lower extremities, both sensory and motor deficits, can lead to muscle wasting, loss of deep tendon reflexes, paralysis of the lower legs, mental confusion, speech difficulties, nystagmus
  • Wernicke Korsakoff
    • Wernicke Encephalopathy: triad of encephalopathy (disorientation, inattentiveness indifference), gait ataxia, and oculomotor symptoms (nystagmus, lateral rectus palsy, conjugate gaze palsies)
      • Triad only seen in 1/3 of patients, most only have around 2.
      • Diagnosis: Clinical but there is a proposed Caine Criteria
        • Dietary deficiency
        • Oculomotor abnrl
        • Cerebellar dysfunction
        • Encephalopathy or memory impairment.
        • 2/4
    • Korsakoff Syndrome: Memory loss, confabulation, +/-hallucinations

Pathophysiology

  • Chronic inadequate intake of thiamine (vitamin B1) leading to degeneration of the peripheral nerves, thalamus, mammillary bodies, and cerebellum.
  • Heart may become dilated, may lead to a high output heart failure
  • Vasodilation can occur causing edema

Diagnosis

  • Clinical history
  • Thiamine level
  • Clinical improvement with thiamine administration
  • CT: May see classic atrophy in the mammillary bodies in Wernicke Korsakoff, highly specific.

Management

  • DO NOT GIVE GLUCOSE 1st, thiamine must be repleted first or else glucose infusions may worsen symptoms. Alcoholics should receive IV thiamine, at least 100mg, before receiving any IV glucose solutions.
  • Nutritional support, thiamine replacement
  • Fix underlying cause (i.e. alcohol)
  • Thiamine initially is given in very high doses if treating, 500mg IV 3 times daily for 3 days, then 250mg daily for 3-5 days, then transition to 100mg PO daily.

Prognosis

  • Most will have a degree of neurological deficits despite treatment.

Hot Topics of 2018!

Today, we reviewed some of the hottest and potentially practice changing articles of 2018.  This is by no means an exhaustive list and meant to encourage debate and tickle your fancy for more!


1. Aspirin for primary prevention of cardiovascular disease?

Bottom line: no net benefit in primary prevention of cardiovascular disease.

  • ARRIVE: 12000 middle aged (mean age 64), non-diabetic participants with moderate ASCVD risk (>20%) randomized to receive aspirin 100 mg or placebo for primary prevention and followed for 5 years. Found that ASA showed no reduction in major adverse cardiovascular events or mortality, but a 2-fold higher risk of bleeding.
  • ASCEND (aspirin): 15000 middle aged (mean age 63) diabetic participants randomized to aspirin 100 mg vs placebo for primary prevention of CVD and followed for 7 years. Authors found a 12% reduction in major adverse cardiovascular events with ASA but a 29% higher risk of bleeding.
  • ASPREE: 19000 older patients (median age, 74) regardless of other risk factors randomized to ASA 100 mg or placebo and followed for 5 years.  Study found that patients who received ASA had a 14% higher all cause mortality, no decrease in the rate of adverse CVD, and no change in disability-free survival.

2. Omega-3 for primary prevention of cardiovascular disease?

Bottom line: potentially beneficial at really high doses in patients with CV risk factors

  • VITAL: 26000 middle aged (mean age, 67) people without CV disease were randomized to receive fish oil (1g) or placebo and followed for ~5 years. Study found similar rates of primary endpoint (nonfatal MI, stroke, or CV-related death) and all cause mortality in the two groups and a small but significant decrease in the incidence of MI in the fish oil group (1.1% vs 1.5%).
  • ASCEND (fish oil): same study population as ASCEND for aspirin, also looked at using 1g fish oil or placebo and followed patients for ~7 years and found no difference in the risk of major adverse cardiac events.
  • REDUCE-IT: 8000 participants with controlled LDL but elevated triglycerides, randomized to receive 2g of a different fish oil (icosapent ethyl as opposed to the eicosapentaenoic acid plus docosahexaenoic acid used in the previous two trials) vs placebo and followed for 5 years.  Study found a 25% reduction in risk of major cardiovascular events. Caveat is high dose used at this formulation is very expensive and the study was funded by Amarin Pharma.

3. VTE prophylaxis in hospitalized patients

Bottom line: High rates of inappropriate use of pharmacologic VTE prophylaxis.  Use padua score before prescribing VTE prophylaxis.

  • Grant et al. JAMA Intern Med 2018: retrospective study of 45000 non-ICU patients hospitalized for > 2 days found that prophylaxis (pharmacologic or mechanical) was prescribed for 78% of low-risk patients. 27% of high risk patients with contraindications to pharmacologic prophylaxis still received it, and 22% of high risk patients did not receive prophylaxis.

4. Is there such a thing as too much oxygen?

Bottom line: higher rates of mortality associated with liberal use of oxygen in hospitalized patients.

  • Chu et al. Lancet 2018: Meta-analysis of 25 randomized trials on 16000 hospitalized patients treated with liberal (median FiO2 0.52) vs conservative (median FiO2 0.21) supplemental oxygenation found that at 30 days, the relative risk of death was significantly higher in the liberal oxygenation group.

5. Plavix + ASA for TIA or minor stroke?

Bottom line: Starting DAPT within 12 hours of symptom onset (likely for 30 days) in patients with high risk TIA or minor ischemic stroke reduces 90 day stroke incidence but increases bleeding rates.

  • POINT:  Followed the earlier CHANCE trial in a Chinese population that showed DAPT for 21 days after TIA or minor stroke reduced stroke recurrence at 90 days without a difference in bleeding rates.  POINT randomized ~5000 patients to DAPT for 90 days vs ASA alone in a primarily white patient population and found lower rates of recurrent stroke but higher rates of bleeding. Majority of stroke reduction occurred during the first 7 days after stroke and extended for 30 days whereas the bleeding rates were stable throughout the 90 day follow up period.

6. Steroids in septic shock?

Bottom line: Steroids might be beneficial in high risk patients with refractory septic shock.

  • Rochwerg B et al. Crit Care Med 2018: Meta-analysis of 42 randomized trials with >10000 patients receiving steroids vs none in septic shock found a 2% relative reduction in 30-day mortality with steroids which was not statistically significant, and a similar reduction in mortality at 60 days to 1 year which reached significance (NNT 50). Reversal of shock at 7 days occurred more frequently in the steroid group (NNT 10) but mild-to-moderate adverse events also occurred more frequently in this group (hyperglycemia, hypernatremia, and neuromuscular disease).

7. Is it safe to discharge to home from the ICU?

Bottom line: patients admitted to the ICU for substance-related disorders, seizures, or metabolic derangements may be ok to go home from the ICU.

  • Stelfox et al. JAMA 2018: retrospective cohort study of 6700 adult patients admitted to ICUs in Canada, 14% of whom were discharged to home, found that 30 day hospital readmissions and ED visits and 1 year mortality rates were similar in those discharged from the ICU vs wards.  Those discharged home were typically younger and more likely to have been admitted due to overdose, seizure, substance withdrawal, or metabolic derangements.

8. NS vs LR?

Bottom line: balanced crystalloids (like LR) are associated with fewer adverse events than normal saline in hospitalized patients.

  • SMART: 16000 patients admitted to the ICU were randomized to NS or a balanced crystalloid (majority received LR). Study found that more patients in the NS group reached the composite outcome of major adverse kidney events (death, renal replacement therapy, or doubling of creatinine at discharge) vs those who received balanced crystalloids.
  • SALT-ED: 13000 patients admitted from the ED to non-ICU beds were randomized to NS vs a balanced crystalloid (majority received LR).  Study found similar rates of primary outcome of hospital-free days but a higher rate of adverse kidney events within 30 days than the NS group.

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:

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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.