Grand Rounds Recap 11.28.18
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Morbidity and Mortality Conference WITH DR. TIM MURPHY
CASE 1: Mycoplasma Induced Rash and Mucositis
Mucositis
Definition: General term for inflammation and ulceration of the mucus membranes (ocular, GU, or GI tract)
Etiology:
Autoimmune
Common in chronic conditions such as Lupus, Pemphigus Vulgaris, Behcet, Crohn’s
Erythema Multiforme- targetoid rash typically triggered by viral reaction
Steven Johnson’s Syndrome- rash with involvement of mucus membranes typically triggered by drugs
Infectious
Mycoplasma induces a rash that is likely separate from SJS or erythema multiforme
Typically also involves ocular findings, unlike SJS
Chemotherapy
3-5 days after infusion of chemotherapy, ulceration at days 6-9
Management
Magic Mouthwash
There is no standardized preparation of this across institutions
Typically contains an antibiotic, antifungal, and a local anesthetic
CASE 2: Rhabdomyolysis
Background
There is no standardized CK level for this disease process. In the literature, typically described as 5x upper limit of normal.
Mechanism is either energy depletion vs direct trauma.
Direct injury to the kidneys can be caused by myoglobin causing tubular obstruction, vasoconstriction due to inflammatory markers, acidic urine.
CK peaks within 2-4 days and decreases in 7-10 days
33% of patients with troponin elevations had false positive troponins (no changes of wall motion abnormalities on echo) in a retrospective review
AST and ALT are frequently elevated because they are found in skeletal muscle
Prognostication
There is a risk score to predict chance of need for hemodialysis and death, but no risk score to help predict admission vs. discharge.
No quality evidence on CK level or Creatinine level which will help decide admission vs. discharge
One can consider discharge if patients can orally rehydrate, if the CK is downtrending, and the overall cause is reversible (eg. athletic training).
Management
Start high volume IVF early
There is no difference between in development of acute kidney injury between normal saline vs. normal saline plus bicarbonate and mannitol vs. lactated ringers
Dialysis should be performed for for refractory hyperkalemia, acidosis, or volume overload
CASE 3: Acute on Chronic Pancreatitis
Common Causes
Gallstones
Alcohol (typically requires drinking 4-5 drinks per day for >5 years)
Medications (sulfasalazine is common)
Diagnosis
Must have 2 of 3:
Lipase elevation
Abdominal pain typical of pancreatitis
CT consistent with acute pancreatitis
Predicting Severity
Classification by 2012 Atlanta Classification
Mild- Absence of organ failure, local, or systemic complications
Moderate- <48 hours of organ failure, local, or systemic complications
High- >48 hours of organ failure, local, or systemic complications
One can use Ranson’s criteria to predict mortality
Risk factor for Mortality
Advanced age
Comorbidities
Obesity
Heavy Alcohol use
BUN >23 equally as sensitive as scores for overall mortality
Necrosis, but CT lags behind clinical findings, and 72-96 hours is when necrosis is typically present
Management
2-4L of fluids over first 24 hours
No benefit to prophylactic antibiotics
ERCP or surgery for gallstone pancreatitis
Drainage only if infection on top of necrosis (rare over first 2 weeks)
Disposition
Admission for patients with signs of and symptoms of end organ damage, inability to tolerate PO, inadequate pain control, patients with gallstone pancreatitis
CASE 4: Lemierre’s Syndrome vs. Mucormycosis with Septic Shock
Lemierre’s Syndrome
Background:
First described in 1936, defined as infectious thrombophlebitis of the internal jugular vein
Classically caused by Fusobacterium necrophorum.
First described in 1936
Treatment:
Broad spectrum antibiotics
Anticoagulation is controversial
Abscess drainage
Diagnosis:
CT scan of the neck with IV contrast
Alternatively, US can be used to evaluate for clot in conjunction with blood cultures
Mucormycosis
Background:
A rare but deadly infection caused by spores from mucomycetes.
Mucor spores inhaled, causing necrotic plaques form in the nasal passages
Populations at risk are patients with DM, cancer, transplant, HIV
Patients on deferoxamine therapy at higher risk due to mucor thriving in iron rich environments
Mortality is ~35%
Clinical Presentation:
Typically presents with acute sinusitis, congestion, nasal discharge, headache
Spreads to contiguous structures including orbit and palate, so thorough HEENT exam is crucial.
CASE 5: Quick Hit- Ant Smoking
Ant Smoking Quick Facts
1/3 of teenagers in Dubai have been approximated to have done this due to a special species of ants in this region
Formic Acid is present in ants, which gives a sensation similar to huffing
North American ants are not known to have the formic acid necessary to give this sensation
CASE 6: Chronic Mesenteric Ischemia
Background:
This is uncommon, has overlapping symptoms with other conditions, and has high mortality
Celiac axis perfuses spleen, stomach, and proximal duodenum.
SMA perfuses from distal duodenum to splenic flexure
IMA perfuses the rest of the large bowel
Etiology:
Occlusive causes include arterial embolism and thrombus, with emboli typically cardiac in origin.
Thrombus as a cause is more common in patient with preexisting atherosclerotic disease
Non-occlusive causes are due to sepsis, heart failure, or dehydration
Diagnosis:
There are no laboratory studies which are sufficiently accurate to identify the presence or absence of necrotic bowel
Lactate is not sufficiently sensitive to rule out this disease (only 85-90% sensitive) in acute mesenteric ischemia
D-dimer is 96% sensitive
Biphasic CTA has sensitivity of 93%, which will show venous and arterial anatomy to rule out venous thrombus
Preliminary studies show ultrasound has a sensitivity of 75%, use your pre-test probability to define your imaging method
Management:
Anticoagulate with a heparin drip
Give broad spectrum antibiotics if concern for bowel ischemia
Reestablish blood flow with embolectomy, angioplasty, or bypass
Surgery for bowel resection is indicated if there is necrotic bowel post reperfusion
Taming the SRU: Tricyclic Antidepressant Overdose WITH DR. KELLI JARRELL
The Case:
A middle aged female of unknown age, unknown PMH presents for AMS. She was found down in a pool of vomit on her couch. FSBG within normal per EMS. She requires a nonrebreather for oxygenation, but vital signs are otherwise stable. GCS of 3 on arrival, so she is intubated with a bougie assisted intubation for airway protection. She has a right mainstem intubation. Tube is retracted.
Husband arrives and reports she took all her amitriptyline pills. However, shortly after his arrival she has hypoxia and suffers a cardiac arrest. ETT suctioning shows obstruction with copious vomit. She gets ROSC after bicarb, calcium, and suctioning.
Post ROSC EKG shows widened QRS, terminal R wave. She is given bicarbonate drip and intralipid, and admitted to the MICU for suspected amitriptyline overdose.
Clinical Pearls:
Altered Mental Status Causes:
Keep a broad differential! Causes include the following:
Abnormal vital Signs
Toxic/Metabolic
Infection/Infarct
Structural (Neurologic structural changes)
Seizure/Psych
Hypoxia in the Intubated Patient
Can use the pneumonic DOPE to decipher causes:
Depth of tube
Obstruction
Pneumothorax
Equipment failure (autoPEEP, ventilator failure)
Tricyclic Antidepressant Overdose
Toxic Effects
Na channel blockade causes RBBB, QRS prolongation, and Ventricular Fibrillation/Tachycardia
Slow K channel blockade can cause QTc prolongation, but torsade is rare
Anticholinergic blockade can cause typical anticholinergic toxicity
Histaminergic blockade causes sedation or stimulation
Nonspecific alpha blockade causes hypotension
GABA blockade can cause seizures and status
Treatment
Bicarbonate intermittent 1-2 mEq/kg boluses until the QRS narrows , with a goal pH of 7.4
Benzodiazepines are first line for seizures
Supportive care for hypotension
Intralipid is recommended for dysrhythmias, hypotension
Calcium Channel and Beta Blocker Toxicity WITH DR. SHAWN HASSANI
Background:
Calcium channel and beta blockers are the number 6 and number 8 cause of tox deaths respectively
Ensure in toxicity you know what did they take, how much, when, and did they take anything else
Workup:
EKG
POC Glucose
Renal
Aspirin and Tylenol Levels
Beta Blockers
Inhibit fast Na channels, causing bradycardia and hypotension
B2 receptors in the lungs cause bronchodilation, so overdose of beta blockers can also cause bronchoconstriction
Typically cause HYPOglycemia
Calcium Channels
Work on the L type calcium channels and cause vasodilation peripherally and have negative inotropic effects in the heart, also causing bradycardia and hypotension
These are protein bound and metabolized by the liver
Typically cause HYPERglycemia
Standard Management
Supportive care including ACLS bradycardia algorithm
Glucagon 5mg IV over 1 minute, may repeat q10-15 x 3 doses
If giving glucagon, pretreat with Zofran as it can cause aspiration due to relaxation of the esophagus
Consider Calcium chloride 10-20 ml of 10% solution for calcium channel blocker toxicity
ECMO can be considered for refractory shock
High dose Insulin
Effective for calcium channel or beta blocker Toxicity
With decreased calcium, body becomes insulin resistant which decreases contractility
The dose is 1U/K bolus and 0.5 1U/KG/Hr infusion up to 10U/Kg/Hr
If glucose <150, give 2 sticks of D50
Give D50 infusion at 100cc/hr to prevent hypoglycemia
Get glucose checks q15-20 min the first hour, then q1hr after that
Vasopressors
Norepinephrine is generally preferred as the first line pressor
Methylene Blue works on endothelial NO synthase instead of adrenergic receptors, so tends to be an effective adjunct to typical pressors
Quarterly SimulationWITH DRs. ROCHE, CURRY, AND FERNANDEZ
Case 1: Aspirin Toxicity with Dr. Conal Roche
22 yo M arrives by ambulance after a fall down stairs. He has a history of depression with recent alcohol intake. EMS found him at the bottom of stairs. Apartment was dirty with many empty alcohol bottles and medicine bottles. Vicodin, Penicillin, and OTC pain medicine (ASA, motrin) were present within the home.
Vital signs reveal tachycardia to 131, stable blood pressure, and tachypnea to 40. He is febrile to 38 degrees Celsius. His exam is remarkable for confusion, slurred speech, and he doesn’t follow commands, but moves all four extremities. No external signs of trauma aside from a forehead abrasion. CT head is negative. VBG shows metabolic acidosis with secondary respiratory alkalosis.
Aspirin levels are high, and renal is consulted, but states he is not a candidate for dialysis. They treat him medically with a bicarbonate drip. Repeat aspirin levels double, so he is taken for hemodialysis and admitted to the ICU.
Critical Actions:
GI Decontamination
Tylenol/Salicylate Levels
Noncontrast Head CT
Alkalanize Urine
Renal consultation for dialysis
Toxicology consultation for recommendations
Case 2: Complete Heart Block with Inferior STEMI with Dr. Woods Curry
75 yo M presents with chest pain and near syncope. EMS reports he was bradycardic to 30s given 0.5 mg atropine and had some improvement to rate of 60s. He arrives with BP in the 80s/60s, heart rate of 60. Glucose is normal. Initial EKG shows complete heart block. He is provided IVF for hypotension, and pads are applied for transcutaneous pacing.
The patient develops pain and repeat EKG shows inferior STEMI. Patient is taken emergently to the cath lab.
Critical Actions:
Fingerstick blood glucose
Pacing with recognition of complete heart block.
Repeat EKG
Cath lab activation for STEMI
Quarterly Simulation with Dr. Fernandez - Rules: Code leader must run the simulation with a blindfold on
The Case:
EMS is called for a middle aged male patient who was found down in his home. On arrival, the patient goes into cardiac arrest with a witnessed arrest. The GCS is 3, ACLS is underway. The patient is then intubated for airway protection, and an arterial line is placed. The patient has wide complex PEA on the monitor on the first pulse check. Cardiac US shows no effusion, no cardiac activity. Given bicarb and calcium, and the next pulse check shows narrow complex PEA. One more round of CPR is resumed and the patient has ROSC. He is started on norepinephrine and admitted to the MICU with undifferentiated shock.
Discussion:
Goal of the Simulation:
Closed loop communication: Being blindfolded led to the need for using names to ensure direct communication and a need for confirmation that an action was performed.
Challenges to closed loop communication:
Task stacking: Requesting one task and then needing something else before the person completes their first task. Can be alleviated through prioritization.
One must have the proper amount of help for critically ill patients. There is a balance between having too many people (having people standing around) and not having enough people.
How to improve teamwork in a code:
Pre-assigning tasks can be helpful to have expectations set. Each person knows what equipment they need, where they need to position themselves in the room, etc. Also allows for a calmer environment at the onset of the code.
It is important to ensure that your thought process has been shared with your team mates but that does not mean that you need to have a ‘’verbal diarrhea’’/ ‘’stream of consciousness”. Finding a balance is important. The end goal is getting your team to anticipate next steps.
