Grand Rounds Recap 11.9.22
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R4 Case follow-up w/ Dr. comiskey
HELLP Syndrome
Epidemiology
Prevalence 0.5-0.9%
30% occurring in postpartum period ~7d
Mortality ~30%
Presentation
RUQ pain, LE edema, abdominal distension, fatigue
Diagnostic Criteria
Platelets < 100
AST > 70
LDH > 600
DIC
Can be seen in 5-56% of HELLP presentations
Etiology
OB Complications (HELLP, placental abruption)
Trauma
Infection
Presentation
Begins with a prothrombotic state
Will progress to hemorrhage as coagulation factors are depleted
Typical Labs
Platelets decreased during hemorrhagic stage
Fibrinogen increased during prothrombotic stage, then decreased during hemorrhage stage
INR elevated
PTT elevated
D-dimer elevated during prothrombotic stage
Diagnosis
ISTHM Criteria
Score < 5 not suggestive of DIC
91% sensitive and 97% specific
Treatment
Supportive care
Transfusions recommended if the patient is actively bleeding or invasive procedure planned
If in the prothrombotic state, heparin may help slow coagulation cascade from progressing
Use TEG to guide balanced resuscitation
R1 clinical diagnostics: Acute liver failure w/ Dr. de castro
Acute Liver Failure: defined by 5 specific characteristics
Severe acute liver injury
Neurologic dysfunction with any degree of hepatic encephalopathy
Impaired synthetic function (INR >1.5)
No prior evidence of liver disease
Disease course of <26 weeks
Used as a cut-off to differentiate between acute vs chronic
Pathology
Hepatocyte function:
Protein synthesis dysfunction → coagulopathy, thrombocytopenia, transaminitis, anemia
Bile synthesis
Carbohydrate metabolism dysfunction → hypoglycemia
Lipid metabolism
Detoxification → if dysfunction → hyperbilirubinemia, hyperammonemia
Etiology
Drugs: acetaminophen, alcohol, amiodarone, amanita phalloides, anabolic steroids, carbamazepine, cocaine, isoniazid, nitrofurantoin, NSAIDs, phenytoin, Reye’s syndrome, statins, sulfonamides, tetracyclines, valproate
Infectious: viral hepatitis, HSV, EBV, VZV, adenovirus, CMV
Vascular: ischemic (shock liver), Budd-Chiari
Pregnancy: AFLP, HELLP
Other: autoimmune, mass/malignancy, heat stroke, sepsis, genetic, Wilson’s, HLH
History: fatigue, malaise, lethargy, confusion, AMS, anorexia, N/V, abdominal pain, distention, pale stools, dark urine, jaundice, itching, lower extremity swelling, bruising, easy bleeding
Risk factors: alcohol use, IVDU, medications, ingestions, toxin exposure, travel history, immunosuppression, family history
Physical exam:
Neurologic exam: mental status, asterixis
Skin: jaundice, lesions
Abdominal exam: tenderness, mass, ascites
Hepatic encephalopathy grading
Grade I: euphoria/depression, mild confusion, slurred speech, disordered energy
Grade II: lethargy, moderate confusion
Grade III: marked confusion, incoherent, sleeping but arousable
Grade IV: coma
Labs: CBC, BMP, Mg, Phos, LFTs, LDH, PT/INR, PTT, TEG, lactate, VBG, ammonia, UA, UDS, pregnancy, APAP, toxicology screen, viral serology, autoimmune panel, HIV
Imaging
Ultrasound: Budd-Chiari syndrome, portal HTN, hepatic steatosis, hepatic congestion, and underlying cirrhosis
CT and MRI more sensitive at diagnosing malignancies
Treatment: depends on cause
Acetaminophen: NAC
Hepatitis B: antiviral
Mushroom poisoning: activated charcoal
Budd-chiari: surgery, thrombolysis
HSV: acyclovir
Wilson disease: PEX, transplant
Autoimmune: steroids, transplant
AFLP, HELLP: delivery of fetus
Supportive therapy
ABCs
IVF, electrolyte replacement
ICP management
NAC
Transplant center
Liver transplant
MELD score is a well established and validated predictive model of short-term mortality in patients with liver failure
Case 1: Acetaminophen toxicity
Stages
Stage I (0-24h post ingestion): anorexia, nausea, vomiting. Hepatic transaminases may start to rise
Stage II (24-74h post ingestion): see improvement in clinical findings, some patients may report RUQ abdominal pain. Elevated AST/ALT, bilirubin, INR
Stage III (72-96h post ingestion): hepatic failure, acidosis, sometimes renal failure and pancreatitis. Peak in AST/ALT, bilirubin, INR
Stage IV (>5 days): progression to multiple organ failure, resolution of hepatotoxicity and survivors
Rumack-Matthew Nomogram
Used to determine the risk of APAP-induced hepatotoxicity after a single acute ingestion (not for chronic or repeated ingestions)
Serum concentrations above the treatment line indicate need for NAC therapy
Treatment line starts at 150 mcg/mL at 4 hours post ingestion
If nomogram cannot be used due to unknown time of ingestion, can use labs to determine risk of toxicity
APAP, LFTs → if elevated or detectable for APAP, treat
APAP undetectable with no LFT elevation → no treatment
N-acetylcysteine (NAC) therapy
Treatment should begin within 8 hours or ASAP
IV (Acetadoate)
21-hour regimen consisting of 3 doses
Loading- 150 mg/kg over 1 hour
Second- 50 mg/kg over 4 hours
Third- 100 mg/kg over 16 hours
Oral (Mucomyst)
72-hour regimen consisting of 18 doses
Loading- 140 mg/kg
Maintenance- 70 mg/kg q4 hours for 17 doses
Repeat dose if emesis occurs within 1 hour of administration
Case 2: Viral Hepatitis
Labs:
IgM: acute infection
IgG: nonspecific, either acute, chronic, or previous infection
HbSAg- current infection
Anti-HbS- previous cleared infection or previous vaccination
HBe- marker of infectivity
Risk Factors
A: ingestion of infected foods, fecal-oral contact
B: bodily fluids, vertical transmission is more common in Asian countries
C: bodily fluids
D: oral replicates in the presence of Hepatitis B, similar risks
E: ingestion of infected foods, fecal-oral contact
Conclusion
Definition
INR >1.5
Neurologic dysfunction with any degree of hepatic encephalopathy
No prior evidence of liver disease
Disease course <26 weeks
The most common cause in ALF in the U.S. is acetaminophen toxicity, treated by NAC
Management
Identification of the etiology and initiation of specific treatment
Supportive and symptomatic management of the ALF, with timely transfer to the critical care unit
Early consultation with liver transplant specialists and transfer
Ultrasound grand rounds
Station 1: Superficial Cervical Plexus Block w/ Dr. Baez
Helpful for doing IJ central lines and can also provide anesthesia around the clavicle for subclavian lines
Where?
Look for SCM and about middle of the neck (not too high, not too low)
Target: superficial cervical plexus
How?
Find IJ like you normally would
Slide posteriorly to find posterior border of SCM
Look for fascial layer (cannot always see nerve bundle) and deposit anesthetic
Only need about 3cc
What could go wrong?
Temporary
If too low, can anesthetize
Phrenic nerve
Recurrent laryngeal
Brachial plexus
Too deep
Horner’s syndrome
Station 2: Transesophageal Echocardiography w/ Dr. Frederick
There are four main movements in terms of probe placement
Withdraw and advance
Rotation forward and backward
Anteflexion and retroflexion
Flexion to the right and left
Prep
Step 1: Intubation
Step 2: Gastric decompression
Step 3: TEE insertion
Step 4: Bite block seating
VIews
Midesophageal 4 chamber
Insert probe to mid-esophagus
Omniplane 0-10°
Cardiac structures: four chambers, mitral and tricuspid valves, and pericardium
TTE equivalent: apical four chamber
Clinical application: pericardial effusion, intraventricular thrombus, LV/RV function, valve lesions and dysfunction
Mid-esophageal long axis
Insert probe to mid-esophagus
Omniplane to ~130°
Cardiac structures: left ventricle, left atrium, mitral and aortic valves
TTE equivalent: parasternal long axis
Clinical application: Quality of CPR, LV function, pericardial effusion, mitral/aortic valve dysfunction
Trans-gastric short
1. Insert probe until you lose the heart and see gastric rugae
2. Anteflex slightly
Cardiac structures: left ventricle
TTE equivalent: parasternal short axis
Clinical application: LV function, regional wall motion abnormalities, pericardial effusion, septal motion
Mid-esophageal Bicaval
Insert probe to mid-esophagus
Omniplane to ~90°
Rotate wrist all the way to the right
Cardiac structures: simultaneous view of the IVC, RA, and SVC
TTE equivalent: N/A
Clinical application: procedural guidance (i.e. ECMO cannulation), volume responsiveness
Station 3: DVT Ultrasound w/ Dr. Minges
Preparation: allow adequate exposure of the groin and positioning of the patient
Linear probe is preferred
First, identify the common femoral vein
Next, scan inferiorly to identify the saphenofemoral junction (which looks like a snail)
Continue inferiorly to find the femoral vein/deep femoral vein (which looks like a snowman)
Last is the popliteal vein
Compress along each point and identify if the vessel is collapsible. A noncompressive vein should raise suspicion for thrombus
Acute DVT tends to be more anechoic, more homogenous, less well attached, and with smooth borders
However, determining the chronicity of a thrombus is not within our scope of practice as emergency physicians
Pediatrics lecture: Neonatal resuscitation in the community w/ Dr. Vinet
NRP vs. PALS
First 24 hours of life = NRP
After first 24 hours = PALS
Fetal Circulatory Anatomy & Physiology
oxygenated blood enters the right atrium from the umbilical vein and crosses to the left side of heart through the foramen ovale and ductus arteriosus
there is only a small amount of blood flow to the lungs, and no gas exchange takes place in the fluid-filled lungs
Transition at birth
Replace alveolar fluid with air
Breathe regularly
Increase pulmonary blood flow
Increase systemic vascular resistance
Decrease pulmonary vascular resistance
Goals of resuscitation = ventilate
85% will breathe in first 30 seconds of life
10% will breathe after stimulation and warming
5% of term infants will require PPV
only 2% require intubation
APGAR Score
7-10 normal
4-6 needs respiratory support
< 4 immediate intervention required
Measured at 1 and 5 minutes of life
Initial management
Rapid assessment
Dry/Warm/Stimulate
ABC’s
O2 goals in the first few minutes of life are different, and it is helpful to have this reference available
Glucose goals are different in neonates (<30 in first 24 hours is abnormal)
Equipment List adapted from ACEP/AAP Policy Statement (not exhaustive):
Warm
warmer
warm towels/blankets
temp sensor
hat
plastic bag or wrap (<32 weeks)
Clear Airway
bulb suction
10-12F suction catheter (80-100 mmHg max)
Auscultate
stethoscope
Ventilate
PPV device/bag
term and preterm size masks
8F OG
LMA size 1 for term
monitor
oxygen blender (21% for term, 21-30% for <32 weeks)
Oxygenate
Pulse ox
chart of target O2 sats
Intubate
laryngoscope with size 0 and 1 straight blade, size 00 is optional
stylets optional
ETT (size 2.5-3.5)
EtCO2
Medicate
epinephrine (1mg/10 mL)
normal saline
UVC supplies
chart for medications
Cord clamp
Differential Diagnosis for respiratory distress
Failure to transition (airway obstruction, hypothermia, poor ventilatory effort, ineffective respiratory support)
Transient Tachypnea of the Newborn
Meconium Aspiration
Respiratory Distress Syndrome (RDS)
Pneumothorax (spontaneous or barotrauma)
Congenital Heart Disease
Congenital Diaphragmatic Hernia (especially if distress worsens with PPV)
Persistent Pulmonary Hypertension
failure to lower PVR after birth, resulting in R -> L shunt
Airway/Pulmonary abnormalities or dysfunction
tracheoesophageal fistula, ciliary dyskinesia
Indications for PPV (after initial steps)
baby not breathing, or
baby gasping, or
baby’s HR is <100 bpm
Give 40-60 breaths/min, FiO2 21-30%
Minimal PEEP (4-5, max 8)
PIP 20
Indications for intubation
HR <100 bpm and no improvement with PPV
Before starting chest compressions
can consider LMA for infant >2kg
Tracheal suctioning for obstruction
Stabilization of a newborn with a suspected diaphragmatic hernia
Prolonged PPV
No need for RSI
Chest Compressions
Indication: HR <60 bpm despite at least 30 seconds of PPV (with good chest rise)
Rate 90, ratio 3:1
Discontinue when HR >60
Consider IV/IO epinephrine if no improvement after 1 minute (can be given endotracheally if necessary)
