Grand Rounds Recap 02.17.21
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MORBIDITY AND MORTALITY with Dr. Koehler
Case 1: Imaging in Ovarian Torsion
Ultrasound is the imaging modality of choice:
Absence/lack of arterial or venous blood flow: sens 85%, spec 37%
Whirlpool sign: sens 90%
Asymmetric ovarian enlargement: sens 85%, spec 18%
**Normal doppler waveform alone cannot exclude the diagnosis
CT imaging may be helpful:
Adnexal enlargement, smooth margins of ovary, adnexal deviation are findings that could indicate ovarian torsion
N=30 pre-operative CT scans for ovarian torsion, 28/30 with associated mass, 22/30 with pelvic fluid, no patient had a completely normal CT scan
Gold standard is still diagnostic laparoscopy - consult gynecology if you have a high suspicion!
Case 2: Access in Cardiac Arrest
Convenience study assessed N=75 obese patients who came into the ED. Ultrasound used to assess soft tissue depth at the proximal humerus, proximal tibia and distal tibia.
Mean BMI 47.2.
Mean soft tissue depth at proximal humerus was 29.6mm, proximal tibia was 11mm, distal tibia was 10.7mm.
Tibial tuberosity palpable in 70 patients (BMI 45.7), not in 5 patients (67.2) who had >20mm of tissue depth
Length of IO needles by color:
Pink 15mm
Blue 25mm
Yellow 45mm
ETT administration of code medications
Adults: NAVEL (naloxone, atropine, vasopressin, epinephrine, lidocaine)
Pediatrics: LANE (lidocaine, atropine, naloxone, epinephrine)
Considerations for ETT medication administration
Need to increase dose by 2-2.5X
Mix with 5-10ml of sterile water (epinephrine and lidocaine may be better absorbed by lung parenchyma when mixed with sterile water than normal saline) or normal saline
Perform 1-2 ventilations while “very briefly” holding chest compressions to allow lung absorption - may be best to do it during pulse checks
Case 3: Orthostasis and Epistaxis
Orthostatic vital signs are generally not helpful, however in acute hemorrhage can be sensitive for significant loss. Absolute numbers vary but patient is symptomatic, assume they are volume down.
Systematic review in 1999 assessed 10 studies involving healthy volunteers who donated blood
Postural tachycardia (increase by 30bpm when standing) and postural dizziness can be used as surrogates for volume depletion
Standing shock index - HR/SBP measurement while patient is standing
N=336 of people who did/did not donate blood
Shock index >0.9 +LR 4.1
Shock index <0.6 -LR 0.5
Check out our clinical guidelines pathway on TTS for epistaxis management!
If using TXA - use pledgets and NOT rhino rockets as TXA can theoretically interfere with polymerization function of rhino rockets
Posterior bleeds will need the longer rhino rocket (7.5cm ant/post versus 5.5cm ant)
Case 4: Blood Culture Contaminants
How to identify a contaminant:
Identity of the microorganism: Coag neg Staph, Strep viridans, Clostridium perfringens, Bacillus spp., Corynebacterium
Coag neg staph is becoming less commonly a contaminant and more commonly a true positive
Prosthetic joint
Central venous catheters
Cardiac hardware
Number of positive bottles
Prospective study of blood cultures in adults (N=940)
Coag negative staph - PPV 3.5% in bottle 1, 61% in bottle 2, 78% in bottle 3, 100% in bottle 4
Difficult to label a positive culture as contaminant in the ED where we oftentimes are only able to get 1-2 cultures
Time to growth
Growth times overlap between contaminants and true infection
Coag negative staph <15 h PPV 84%, >20h likely to be a contaminant
Does not hold true as our technology gets better
Case 5: Posterior Reversible Encephalopathy Syndrome (PRES)
Presenting symptoms
Encephalopathy 50-80%
Seizures 60-75% (status in 5%)
Visual disturbances 33%
Headaches 50%
Risk factors
Renal failure, blood pressure fluctuations, cytotoxic drugs, autoimmune disorders, pre-eclampsia
Diagnosis:
Brain MRI - vasogenic edema in parietal/occipital region, watershed zones, frontal sulcus - best seen on T2 MRI
*Can be seen on CT head with hypoattenuation in the above regions
+Suggested diagnostic criteria:
Acute onset neurologic symptoms
Focal vasogenic edema on neuroimaging
Reversibility of clinical and/or radiologic findings
LP can exclude other diagnoses (meningitis/encephalitis)
EEG does not have specific findings, but can diagnosis status epilepticus
Serum diagnostics are not particularly helpful
Management
Aggressive BP management - decrease MAP by 25%, SBP <180
No particular antihypertensive that is preferable in this case (can use nicardipine, labetalol, etc.)
Antiepileptic management - no consensus on prophylactic administration
Given that seizures are prevalent in 60-75% of these patients, have a low threshold to administer antiepileptics (levetiracetam)
Case 6: Cardiac Arrest in Pregnancy
Pregnancy-related mortality in the US has been increasing over the past few decades - may be due to increased reporting or increasing maternal age
Causes of maternal death (maternal mortality review information app data)
Infection 9.5%
Cardiovascular 12.7%
Hemorrhage 12.7%
PE 9.5%
Cardiomyopathy 11.4%
AHA Guidelines for Cardiac Arrest in Pregnancy
12-14 weeks: uterus can begin to compress IVC/aorta and affect hemodynamics in pregnancy - increases afterload and decreases cardiac return
20 weeks: decreased ejection fraction when uterus compresses on IVC/aorta
Decreased functional residual capacity as uterus presses up and compresses diaphragm - FRC decreases by 10-20%
Less hypotension with MANUAL DISPLACEMENT of uterus off IVC/aorta when compared to 15 degree left lateral decubitus tilt!
AHA currently advises against use of mechanical chest compression devices (i.e. Lucas) in pregnant patients - no current studies available
Perform a perimortem C-section within 5 minutes of witnessed arrest in pregnancy
>20w gestation
Palpable fundus at the level or above the umbilicus
Higher fetal survival at >30w compared to >24w
Please refer to TTS (https://www.tamingthesru.com/blog/air-care-orientation-curriculum/resuscitative-hysterotomy) for more information on how to perform a perimortem C-section/resuscitative hysterotomy
Case 7: Cervical Myelopathy
Physical exam findings and symptoms are subtle - so keep a high index of suspicion for this disease process
Symptoms: neck pain, paresthesias into arms, difficulty with fine motor control in hands, gait disturbances, Lhermitte’s sign
Physical exam findings:
Hoffman Sign can be used to assess for upper motor neuron lesion or corticospinal pathway dysfunction
3% of the general population can have this without neurologic pathology
+LR 2.6, PPV 94.6%
Finger escape
Grip and release
ATTENDING CASE FOLLOW-UP with Dr. McMullan
Our patients are people, not our problems. It is OK to have complex emotions and personal connections in complex cases.
R1 CLINICAL KNOWLEDGE: CYANIDE & CARBON MONOXIDE TOXICITY with Dr. Wosiski-Kuhn
Smoke inhalation is the most common cause of death in fire-related mortalities (50-80%)
Cyanide Toxicity
Fire in an enclosed space is the #1 risk factor for cyanide (CN) toxicity
Etiologies:
Cyanogenic glycosides (pitted fruits - cherries, apples, plums, peaches), sodium nitroprusside are also causes of CN toxicity.
Bitter almond smell has sensitivity 4-18%
Clinical presentation
Inhalation of hydrogen cyanide gas - rapid LOC and seizures
Acute ingestion of cyanide salts - GI symptoms within 40 mins
Acute exposures: sympathetic activation -> depression -> coma, death
Chronic exposures: headache, weakness, pruritic rash, chest, abdominal pain
Resuscitation pearls:
ABC
Suspect cyanide toxicity - decontaminate
Call for help
Co-ingestion labs, EKG, LFTs (cyanide is metabolized by liver), VBG
*Lactate > 8mmol/L has 94% sensitivity for cyanide toxicity
Early oxygen administration redistributes cyanide from intravascular compartment to intracellular compartment, and also assists in augmenting antidote effects
Antidotes:
Cyanokit (hydroxcobalamin) - forms B12 that allows renal excretion
Onset of action 5-10mins
IV only, expensive, moderate transient hypertension, AKI
Causes pink discoloration of skin and bodily fluids for weeks to months
Has effect on many serum values (magnesium, creatinine, etc.)
Adult dose 5g in 200ml 5% dextrose IV over 15-30mins
Peds dose 70mg/kg up to 5g IV
Give every 15 minutes as clinically indicated
FDA approved in pregnancy
Alternative therapies: amyl nitrite - inhaled capsule, sodium thiosulfate
Disposition
Asymptomatic + normal blood gases: 6hr observation, discharge
Minimal symptoms: admit to observation, supportive care
Acute poisoning: stepdown v ICU admission
Poisoned from nitriles or poorly soluble salts: 24h observation
Carbon Monoxide Toxicity
Carbon monoxide is #1 cause of death by poisoning in the US
Etiologies
Gas power tools, car exhaust in enclosed space, portable heaters/gas-containing ovens with poor ventilation
Methylene chloride (in paint strippers) is metabolized to CO by liver
Toxicity mechanisms - impaired oxygen delivery, disrupted cellular respiration, direct cellular damage
CO has 200 times binding affinity for hemoglobin compared to oxygen -> tissues do not undergo aerobic metabolism -> production of lactate and anaerobic energy use
Clinical presentation:
Clinical effects within 2 hours of exposure
Present with headache, dizziness, nausea, vomiting, chest pain, fatigue, syncope
Cherry red lips is not a common finding
Diagnosis:
CMP, CK, VBG, lactate, pregnancy test, CXR, EKG, hs-T, carboxyhemoglobin levels (although normal COHb does not exclude CO poisoning as patient’s levels can rapidly drop once removed from the culprit environment)
COHb >2% in non-smokers
COHb > 9% in smokers
*False positives can occur in hemolytic conditions (sickle cell, hemolytic anemia)
Cognitive assessment - mini mental status - to document changes in clinical course
Severe metabolic acidosis is associated with short-term mortality, lactate does not
Treatment and disposition
Oxygen - administer oxygen in an attempt to flush out CO
Half-life of CO at room air is 4-5 hours; 90mins with oxygen delivered via NRB; 20-30mins with hyperbaric chamber therapy
Indications for hyperbaric chamber therapy:
CO co-ox level >25% (>15% if pregnant or child)
LOC or cardiovascular compromise
pH <7.1
End organ damage
Non-invasive positive pressure ventilation may help en route to hyperbaric chamber/pre-hospital settings
Delayed neurological sequelae
Chronic headache, mood disorders, personality changes, memory loss, focal neurologic deficits
40% of patients
No correlation with initial CO level
Pediatric patients have higher morbidity at even lower CO levels, higher metabolic rates and immature CNS, initial exposure can be underestimated
R3 TAMING THE SRU with Dr. Roblee
Tele call: Elderly male, altered mental status, hypotensive
On presentation to ED: hypothermia, tachypnea, hypotension, ETCO2 10. On exam, patient is alert to self and place, however unable to say why he is in the ED. PMH notable for CAD s/p stents, HTN, hypercholesterolemia, ETOH use
Pearl #1: If the patient’s end tidal is really low, it’s usually really bad.
The amount of CO2 in the blood is an indicator for cardiac output and perfusion...if it’s low, perfusion is low or they are compensating for a significant acidosis, or both.
Patient has a cardiac arrest and receives epinephrine, bicarb, and calcium. VBG demonstrated worsening acidosis, and a sodium bicarb and epinephrine infusions are started. ROSC is achieved. Patient is ultimately admitted to the MICU where his hemoglobin finally results at 3. Provided with pRBCs. No TTM given response to commands, has rapid improvement in symptoms within the first few hospital days. Reports significant alcohol use, ibuprofen use, and coffee ground emesis prior to presentation to ED.
Pearl #2: Hemorrhagic shock
This patient had renal failure -> uremia -> severe metabolic acidosis
This patient also had poor perfusion -> lactic acidosis -> severe metabolic acidosis
Severe metabolic acidosis was likely the etiology of his cardiac arrest
Acidosis leads to decreased cardiac output, decreased response to catecholamines, and arrhythmias
Pearl #3: Considerations with sodium bicarbonate administration:
1 amp of bicarb is extremely hypertonic (equivalent to 8.4% NS)
May transiently worsen intracellular acidosis
BICAR-ICU trial was an open-label, multicenter RCT. N~400 patients with severe metabolic acidosis (pH <7.2) were randomized to either receive 4.2% bicarb infusion with a goal pH of 7.3, or to receive no bicarb.
No difference in all cause mortality between bicarbonate and control groups
Pre-specified subgroup analysis demonstrated that patients with more severe AKI had a significant mortality benefit when receiving bicarbonate than control group
Patients who receive bicarbonate had a lower need for renal replacement therapy than control group
R4 CAPSTONE with Dr. Lane
Contribution margin
Revenue = profit + costs
Costs = fixed + variable
Why what we do is special:
Have to be open 24h/d
Have to serve any need
Have to serve any customer
Lower tolerance for any service level impairment
Facility requirements are specialized
Equipment is specialized
Labor is specialized
Revenue = recurring revenue + transaction based revenue
Revenue = contribution margin + variable cost
Contribution margin = fixed cost + total margin
Summary Points:
We can make a big difference with small changes
Making small, simple improvements in the clinical environment you work in can benefit patients and be rewarding
Run toward what you fear in residency
Communicate as well as you can
And - in the future - pay attention to financial discussion because this is essential to serving our patients
Values
Safety - what is the safety way to accomplish a task
Clinical excellence - what is best for the patient
Financial sustainability and growth
