Grand Rounds Recap 8.31.22

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morbidity and mortality with Dr. broadstock

Metformin-induced Lactic Acidosis

  • Metformin is a biguanide derived from French lilac plant

  • 90% of the drug is renally excreted so FDA does not recommend Metformin use for patients with Cr >1.5 or GFR <50

  • Metformin-induced lactic acidosis

    • MALA: Metformin Associated Lactic Acidosis- patient is on Metformin but has concurrent pathology that could attribute to rise in lactate (shock, hepatic failure, etc) and presence of Metformin may exacerbate lactic acidosis

    • MILA: Metformin Induced Lactic Acidosis- no other observable cause for lactic acidosis so acidosis thought to be attributable to use of Metformin 

  • Presentation

    • Decreased pH

    • Increased lactate

    • May also see hypothermia, refractory vasoplegia, GI symptoms, delirium

  • Treatment therapies

    • Initial Resuscitation

      • Supportive care is mainstay of therapy

      • Isotonic bicarbonate can be considered if pH <7.2 with hemodynamic instability

      • Lactate in LR cannot be metabolized due to altered biochemistry

      • Consider D5W with ½ NS plus one ampule (50 mEq) of bicarbonate

    • Renal Replacement Therapy: one of the mainstays of treatment

      • Consider renal replacement therapy for patients with lactate >20, pH <7, shock, or decreased level of consciousness

    • Insulin and Glucose Therapy: may be beneficial for Metformin overdose by facilitating glucose utilization, sustaining glycolysis, mitigating hypoglycemia, attenuating breakdown of fats and lipids

    • Methylene Blue: can obtain electrons from NADH and donate to cytochrome c in the mitochondria (bypassing Complex I in electron transport chain). Also functions to decrease nitric oxide production and improve vasoplegia

      • 2 mg/kg loading dose over 15-30 min followed by 0.25 mg/kg/hr infusion

  • Case Summary

    • Metformin induced lactic acidosis is a rare entity, but should be considered for patients with significantly elevated lactic acidosis and metformin therapy

    • Consider renal replacement therapy early in patients with pH <7, lactate >20, altered mental status, or hemodynamic instability

    • Reserve bicarbonate, insulin, and methylene blue for patients in shock or refractory to other therapies

    • Retail Rx Dispense is a useful tool to verify medications being filled

Spontaneous Intracranial Hemorrhage

  • Repeat head CT: in patients with spontaneous ICH with stable examination and preserved level of consciousness, follow up head CT at 6 and 24 hours after onset appears adequate to exclude hematoma expansion

  • Spontaneous ICH admission to a stroke unit vs medical ward

    • Mortality benefit and improved 3-month functional outcomes for patients admitted to stroke unit or specialized unit over medical ward

  • In spontaneous ICH, repeat head CT scans are warranted to monitor for hematoma expansion, as they have a higher likelihood of expansion compared to traumatic ICH

  • Patients with spontaneous ICH should be admitted to a stroke unit for specialty care

Traumatic Hemopericardium

  • Hemopericardium can be difficult to detect in cases in which the blood is clotted and appears more isoechoic to the liver and myocardium

  • Prevalence of hemopericardium

    • Penetrating trauma: 11-13%

    • Blunt trauma: 0.06%

  • Blunt hemopericardium is a rare entity

  • Clotted blood has similar echogenicity to cardiac tissue

Bacteremia and Outpatient TPN

  • Incidence 0.37-4.6 episodes per 1000 catheter days

  • >50% gram positive bacteria

  • 14% fungal species: typically antifungal therapy is not recommended unless the patient is presenting with septic shock or is immunosuppressed in addition to receiving TPN therapy

  • Risk factors for outpatient TPN line infection

    • Risk for implanted port > tunneled catheter

    • Frequency of access- higher risk for infection

    • Family member is primary caregiver → higher risk of infection

    • Duration > 250 days

  • Line-associated Infection

    • 2 blood cultures- one from peripheral source and one from the line itself

    • If unable to obtain peripheral cultures, obtain two blood samples drawn through different catheter lumens

  • Patients with fever on outpatient TPN have a higher incidence of bacteremia

  • Peripheral and line cultures should be obtained in febrile patients with long term catheters

  • Culturing all ports from indwelling line increases test sensitivity

  • Bacteremia may be subtle in these patients

Hypertrophic Obstructive Cardiomyopathy

  • How do we define HOCM? 

    • Myocardial wall thickness >15 mm. Obstruction is present in 40-70% of these patients.

  • Bernoulli's principle: pressure of a fluid is inversely proportional to the speed at which it is traveling. Speed is inversely proportional to cross sectional area of the vessel

    • LV hypertrophy → cross sectional area of space is decreased → fluid pressure decreases as speed increases, therefore generating a low pressure area towards the LVOT which pulls the anterior leaflet of the mitral valve upward causing an obstruction of blood exiting the heart

    • This abnormal movement of the anterior valve leaflet causes incompetence of the valve leading to mitral regurgitation and pulmonary edema

  • LVOT Obstruction: Systolic anterior motion of mitral valve = SAM physiology

    • Impairs ejection of blood into aorta by mitral valve leaflet

  • Dynamic LVOT Obstruction can also be seen in Takotsubo cardiomyopathy, LAD ischemia with apical hypokinesis, hypertensive cardiomyopathy, distributive shock with volume depletion

  • Factors that worsen LVOT obstruction

    • Increased inotropy: increased contractility will increase flow of blood out of the LVOT, worsening pressure gradient

    • Increased chronotropy: decreases ventricular filling time causing smaller stroke volumes and worsen LVOT crowding

    • Volume depletion and poor preload

    • Diuretics, inotropes, and vasodilators will WORSEN LVOT obstruction

  • Management: directed at maximizing filling of ventricles, maximizing preload, maximize diastolic filling time

    • IV Fluids

    • Heart rate control- esmolol is a good choice

    • Peripheral vasoconstriction: phenylephrine, vasopressin

  • HOCM can predispose patients to dynamic LVOT obstruction, which is a rare cause of cardiogenic shock

  • LVOT obstruction is worsened by many of the traditional therapies we use to treat cardiogenic shock

  • Goals of therapy include maximizing preload, increasing ventricular filling time and minimizing exogenous inotropy

  • Consider LVOT obstruction in your differential for shock that is refractory vasopressors and inotropes

tPA for Suspected Pulmonary Embolism During Cardiac Arrest

  • If you decide to administer thrombolytics, you must continue CPR for a duration of time to circulate tPA

  • There is no standard recommendation for duration with some guidelines recommending 15 minutes up to 90 minutes. Our local practice is 20-30 minutes.

  • CPR = 50 mg push (can repeat 50mg in 15 minutes)

  • Unstable = 10 mg push + 90 mg over 2 hours

  • tPA can be effective for patients with PE who suffer cardiac arrest

  • Continue CPR for at least 30 minutes following administration of tPA

r3 Small Groups with Drs. Milligan, Yates, and gillespie

Thoracentesis with Dr. Milligan

Indications for Thoracentesis  

  • Therapeutic: Pleural effusion + Respiratory distress (new oxygen requirement, worsening dyspnea) 

    • Removal of compressive effusion fluid allows for lung re-expansion, improved V/Q matching  

  • Diagnostic: New pleural effusion of uncertain etiology  

Safety Concerns/Complications 

  • 1-3% risk of pneumothorax with ultrasound guidance 

  • ~2% risk of bleeding (chest wall hematoma, hemothorax), no absolute contraindications for coagulopathy or thrombocytopenia 

  • <1% risk of intra-abdominal injury with ultrasound guidance 

  • <1% risk of re-expansion pulmonary edema 

    • Negative pressure generated from removing pleural fluid and re-expanding lung may cause inflammatory response at the pulmonary capillary that leads to pulmonary edema  

    • Weakly correlated with volume of removal >1500 mL 

      • Guidelines recommend removing <1500 mL for this reason 

      • For most therapeutic procedures only need to remove 500-1000 mL for improvement in symptoms  

    • Higher risk with higher negative pressures generated from vacuum bottles, recommend gravity or syringe pull techniques for large-volume removal 

Equipment 

  • Thoracentesis Kit 

    • At UC lives in carts by A1, bottom shelf 

    • Contains catheter over needle with self-sealing valve, when needle withdrawn valve closes so air cannot enter pleural cavity 

    • Catheter fused to stopcock  

    • Tubing with one-way valve that allows you to withdraw/pull fluid with included 60 cc syringe and then push it into collection bag without manipulating catheter or stopcock  

Landmarks 

  • Sitting (patient leaning over bedside table)  

    • Mid-scapular line below inferior edge of scapula 

  • Supine (with head of bed elevated as much as possible) 

    • Posterior axillary line, inferior to nipple line 

  • Exact rib space will be determined by location of diaphragm, lung, and effusion on ultrasound 

  • Ensure you are going to be entering directly over the rib to avoid hitting intercostal vessels  

Thoracentesis Technique 

Finding Your Spot 

  • Use curvilinear probe in longitudinal orientation relative to long axis of body to evaluate intercostal spaces for location of lung, effusion, and diaphragm  

  • Watch for lung and diaphragmatic excursion during respiratory cycles 

  • Want to be near deepest point of effusion without hitting lung or diaphragm 

  • Can measure depth of effusion from chest wall to determine depth of needle insertion 

  • Mark your preferred intercostal space (cap of needle works well similar to LP) 

Preparation 

  • Prep skin with chloraprep, apply sterile drape 

  • Anesthetize skin with lidocaine by making a skin wheal then aspirating as you advance and inject in same trajectory you expect to insert needle, directly over the rib, okay if you reach pleural fluid as you will be helping anesthetize parietal pleura which is often most sensitive part 

  • Make a skin nick to allow for passage of catheter 

Insert Catheter over Needle 

  • Put 10 cc syringe on end of catheter as you advance directly over top of rib, continuously aspirate until you reach pleural fluid 

  • Can do this under real-time ultrasound guidance

    • Linear or curvilinear probe in longitudinal orientation, in-plane technique  

    • Linear probe in longitudinal orientation, out-of-plane  

  • Once you’ve reached desired depth and are aspirating fluid, withdraw needle and disconnect 10 cc syringe which will close the self-sealing valve  

    • If you are not using thoracentesis kit, be sure to immediately cover needle after you remove syringe to avoid causing a pneumothorax  

  • Attach tubing to lure lock, 60 cc syringe will attach to lure lock midway of tubing beyond one-way valve 

  • Make sure stopcock is open to patient and tubing 

  • Aspirate pleural fluid with 60 cc syringe, pushing fluid back in from syringe will push it into collection bag rather than back into patient 

  • Continue aspirating and filling bag until you’ve removed desired volume 

Remove Catheter  

  • Withdraw catheter quickly, apply an adhesive dressing 

  • Check for pneumothorax with ultrasound or CXR  

Send Fluid for Analysis 

  • Basic Labs: Cell count, glucose, pleural protein, LDH, Gram stain, culture 

  • Light’s criteria: If fluid meets any of the following consistent with exudative effusion (sensitivity 91%, specificity 76%):  

    • Pleural protein > 50% of serum protein 

    • Pleural LDH >60% serum LDH or >2/3 serum upper limit of normal  

  • Normal fluid should be straw-colored and clear, cloudy or darker fluid can be signs of exudative effusion 

Taming the Transducers (Lung Ultrasound) with Dr. Yates

  • 4 pathologies that can be diagnosed with lung ultrasound and have an equal to or better specificity/sensitivity than chest x-ray:

    • Pneumonia/Consolidation

      • Can be seen best at the PLAPS point

      • Signs that indicate pneumonia: Shred sign, focal B-lines, Hepatization of the lung (need to rule out mirror artifact which is normal), Bronchograms (dynamic air are most specific) 

    • Pneumothorax

      • Often will use linear probe to look for this if clinical suspicion, best view of the pleura

      • Lung sliding is the normal finding indicating no pneumothorax at the area being reviewed by the probe. Can be better visualized on M-mode and will create a "Sandy Beach/Seashore" sign

      • Finding the lung point, where the lung separates from the parietal pleura and there is a stoppage of lung sliding, is highly specific for pneumothorax. Can be better visualized on M-mode and will create a "Barcode" sign

    • Pulmonary Edema

      • Normal findings with no fluid on the lung are A-lines (horizontal reverberation artifact) and Z-lines (short comet tails that do not stretch across the screen or cancel or A lines)

      • Diffuse B lines are highly specific for pulmonary edema. These must arise from the pleural line, stretch across the screen, will cancel out A lines, are hyperechoic, and move with lung sliding 

    • Pleural effusion

      • Also best seen with PLAPS point

      • Signs that indicate this: spine sign, quad sign, sinusoid sign

Best transducers to use for complete lung ultrasound: Curvilinear if the patient's anatomy allows, otherwise Phased-array is a good second option for maneuverability between ribs.

Taming the Tracheostomy with Dr. Gillespie

  • Why do we care about this topic 

    • Common ED presentation  

    • Often, if not always seen on ICU rotations  

    • Manipulating tracheostomies incorrectly can cause patient harm  

    • Need to know when appropriate to consult a specialist, and when to conserve that resource  

    • Important to be able to distinguish when a seemingly small issue is not actually a small issue, such as a herald or sentinel bleed (TIF) 

  • Know the anatomy as different than a cricothyroidotomy – often placed at the 2nd or 3rd tracheal rings, more inferiorly  

  • There is an especially important caveat to all artificial airway/non-native airway patients: total laryngectomy or not  

    • Total laryngectomy patients do not have an available, intervenable airway from above to act upon if in respiratory distress and unable to utilize the stoma pathway  

  • Know the parts of a tracheostomy tube  

    • Pilot balloon 

    • Flange/face plate  

    • Cuff 

    • Inner cannula 

    • Obturator  

  • Geometries – basic  

    • Standard 

    • Proximal XLT, for example 

    • Distal XLT, for example  

    • Nomenclature for numbering – manufacturer dependent, can be inner diameter of tracheostomy tube  

    • Fenestrated or non-fenestrated (implications for airflow and phonation possibility  

    • Low pressure, high volume vs high pressure, low volume  

      • Ensure you know by manufacturer whether inflate with H2O or air  

  • Other devices to know 

    • Caps  

    • Speaking valve / Passy-Muir  

      • One-way inhalation valve – prevents expiration through tracheostomy/stoma to redirect airflow cranially for phonation capability  

    • T Tubes  

      • Soft, pliable stents; have superior/cranial and inferior/caudal limb intra-tracheally and external limb that may or may not be capped 

      • Know difficult to remove if absolutely necessary  

      • Know challenges related to from-above airway management given superior extension/limb  

      • Can bag through these using ETT adapter  

  • Basic complications – differ in etiology and anatomy by timeline relative to placement of the tracheostomy  

    • Bleeding  

      • Early vs late 

      • “Early” definition varies – generally, within 7-10d of surgical procedure  

      • Early – suction trauma, surgical bed, tracheitis  

      • Late – often suction trauma, tracheitis, dreaded tracheoinominate fistula  

        • Herald/sentinel bleed can be somewhat subtle prior to true TIF bleed 

    • Decannulation  

      • Early – know must proceed with extreme caution to replace tracheostomy tube given high risk for false passage in recent postoperative period. Recommend consultation, and only if absolutely necessary, Seldinger technique with fiberoptic endoscope for direct visualization  

    • Obstruction  

      • Utility of suctioning, inner cannula, and troubleshooting steps  

  • Evaluation of any patient with a tracheostomy – the “3 W’s”  

    • Why, when, what  

      • Why: why did they have it placed? What was the initial indication? Helps to troubleshoot what you could run into if malfunctioning  

      • When: implications for late vs early / recently placed trach 

      • What: what do they have for the manufacturer, model? Do you have back-ups in place? Whether cuffed or uncuffed? Have there been any problems or complications in the past?  

      • Algorithm for evaluation: from paper cited below 

        • McGrath BA, Bates L, Atkinson D, Moore JA; National Tracheostomy Safety Project. Multidisciplinary guidelines for the management of tracheostomy and laryngectomy airway emergencies. Anaesthesia. 2012;67(9):1025-1041. doi:10.1111/j.1365-2044.2012.07217.x 

  • Random tips and tricks  

    • Can use pediatric mask or LMA as a seal over stoma to bag

Functional movement disorders with dr. eltatawy

  • 10-20% with true epilepsy can have PNES

  • Weakness

    • Hoover’s sign: best sensitivity and specificity, but still poor

    • Collapsing weakness

    • Arm drift before pronator drift

    • Pseudoptosis

    • Wrong way tongue deviation

    • Sternocleidomastoid strength: one of the last things to go. Should be able to turn your head still with weakness

    • Co-contraction: if you are truly working hard (example- flexing arm), the opposite muscle group should relax (i.e. when flexing the biceps, the triceps should relax)

    • Arm drop-face

    • Sedated improvement: functional neurologic deficits often improve after sedation, and it can be helpful to re-examine patients after they have received sedation/anxiolysis (i.e. for MRI)

    • Caveat- pain may increase tone, anxiety can increase reflexes. Patients may exaggerate a real deficit. Look for unilateral reflexes if concerned for UMN

  • Sensory Exam

    • “Midline splitting”: exact splitting of sensation at midline is thought to be functional

      • Caveat: thalamic strokes

    • Splitting of vibration: whether they feel vibration at all

    • Vision loss

      • Optokinetic drum

      • Visual fields: homonymous hemianopsia vs unilateral vision loss

  • Seizures: PNES vs Epilepsy

    • More common with PNES than epilepsy: situational onset, gradual onset, precipitated by stimuli, convulsions >2 minutes, rapid post-ictal reorientation

    • Tongue biting on side is more common with epilepsy whereas tongue biting on tip is more common in PNES

    • Ictal crying and vocalization is more common with PNES

EMS Grand Rounds with Dr. Davis

  • >650,000 sudden cardiac arrests per year with >350,000 out of hospital cardiac arrests (OHCA)

  • 2-3x more likely to survive with bystander CPR

  • Physiologic timeline of cardiac arrest

    • Time 0: cardiac arrest

    • 1s: clinical death

    • 10s: decreased oxygen to brain

    • 5m: depleted glucose in brain

    • 10m: multisystem organ failure

    • 15m: fatal acidosis

    • 15m: biological death without intervention

  • Chain of survival

    • Activation: bystander recognition of medical emergency, 911 call, recognition of medical emergency by 911 call taker, immediate dispatch of first responders or EMS

    • High quality CPR

    • Defibrillation if VF/VT

    • ALS

      • EMS

      • ED

    • Post-ROSC

      • ICU Care

  • Many factors play into outcome of cardiac arrest

    • Non-modifiable risk factors:

      • Patient age

      • Comorbidities

      • Presence of a bystander with witnessed arrest

    • Modifiable risk factors resulting in more favorable outcomes

      • Early CPR (studies have shown improved survival with CPR within 4 minutes)

      • Early defibrillation

  • OHCA Survival Data

    • Increased survival with early CPR and defibrillation

    • More likely to survive if initial rhythm is VF/VT

    • Twice as likely to survive OHCA if in public as opposed to home

    • Higher rate of survival if EMS arrives within 8 minutes

  • What is TCPR?

    • Telephone CPR (TCPR) or Dispatcher Assisted CPR (DA-CPR)

    • Goals:

      • Early recognition

      • Rapid dispatch

      • Pre-arrival instructions: CPR, AED

  • Anatomy of a 911 call

    • First two questions to obtain demographics: location (necessary for dispatch/response) and callback in event of call failure

    • 3rd is to allow a few seconds for caller to say what they think is happening

    • Last two questions are to identify if a patient is in cardiac arrest

      • Is the patient conscious?

      • Breathing? Agonal breathing = ineffective breathing

  • Agonal Breathing

    • Definition by the NIH: an abnormal breathing pattern originating from lower brainstem neurons and characterized by labored breaths, gasping, and often myoclonus and grunting

    • Studies have shown 40% of OHCA present with agonal breathing

  • 5 Take Home Points

    • OHCA survival rate is <10%

    • 10% increase in mortality for every minute without CPR

    • No-No-Go: rapid recognition and dispatch is critical to survival

      • If the patient is not conscious and not breathing normally, high likelihood that the patient is in cardiac arrest and would benefit from CPR

    • Survival benefit with early CPR and defibrillation

    • TCPR increases bystander CPR rates