Grand Rounds Recap 1.15.20
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QI/KT: Tumor Lysis Syndrome WITH Drs. Hunt and Pulvino
Background
Results from the lysing of tumor cells, typically in response to chemotherapy although can be spontaneous as well
Lysis of cells leads to hyperkalmia, hyperphosphatemia, hypocalcemia, and hyperuricemia
In-hospital mortality reported 14-21%
Independent predictors of mortality include dysrhythmia and sepsis
Average hospital LOS 8 days with mean charge of approximately $72,000
This is the most common oncologic emergency and the incidence is rising
Risk factors
Cancers with high rates of turnover, such as leukemia or lymphomas
High tumor burden
Baseline elevated uric acid levels
Pre-existing renal dysfunction
Pathophysiology
Potassium is released from intracellular stores and can lead to dysrhythmia
Phosphorous binds to calcium causing hypocalcemia, resulting in seizures, nausea, vomiting, and weakness
Calcium phosphate crystals precipitate in the kidneys causing acute kidney injury
Higher uric acid also leads to renal vasoconstriction, worsening kidney perfusion
Diagnosis
Presentation
Diagnosed cancer or presentation concerning for new diagnosis of cancer
Renal failure or volume overload
Signs and/or symptoms of hyperkalemia, hypocalcemia, hyperphosphatemia, or hyperuricemia
Often, though, patients present with just generalized fatigue, nausea, and vomiting
Diagnostic evaluation should include
CBC
BMP
Uric acid
Phosphorous
LDH
Hepatic panel
UA
EKG
Simplified Cairo Definition (meets criteria for 2 of the following + diagnosed cancer within 3d before or 7d after chemotherapy)
Uric acid > 8 or 25% increase from baseline
Potassium > 6 or 25% increase from baseline
Phosphorous > 4.5 or or 25% increase from baseline
Calcium < 7 or 25% decrease from baseline
Treatment
Urinary alkalization is no longer recommended as therapy
Allopurinol
Given to intermediate-risk patients: those with highly-sensitive solid tumors and low-grade leukemias and lymphomas
Does not reduce uric acid that is already produced but decreases production
Typically is started before chemotherapy and given after completion of induction chemotherapy
Can cause AKI and interact with other drugs
Rasburicase
Given to high risk patients: high tumor border, high white count, pre-existing renal dysfunction, high grade leukemias and lymphomas
Promotes degradation of uric acid
No difference in response when combined with allopurinol
Time to uric acid control: 4 hours vs. 27 hours with just allopurinol
Adverse events 4%
Expensive!
Reduces incidence of Tumor Lysis Syndrome, AKI, and need for CRRT
Dosing 0.2 mg/kg daily for 5-7 days but can start with single dose of 3mg for uric acid levels 8-12 and 6mg for uric acid levels greater than 12 with additional dosing if needed
Sustained response has been found to be higher in daily dosing
Absolute contraindication for patients with G6PD deficiency
Treatment for Established Tumor Lysis Syndrome
Hyperhydration
5-6 L per day, start with 2 L in the ED
Target goal UOP of 2 cc/kg/hr
Can increase UOP with loop diuretic as needed
Hyperkalemia
Only given calcium for EKG changes
Bicarbonate only for EKG changes or K > 7
Otherwise, typical care, including insulin, albuterol, and kayexelate
If refractory, consider hemodialysis
Hypocalcemia
Replete only if symptomatic (tetany, seizures, delirium, arrhythmia) with the lowest possible dose
Most importantly, treat hyperphosphatemia
Hyperphosphatemia
Aggressive fluid hydration
Phosphate binder therapy
If greater than 7.5 or refractory, consider dialysis
Hyperuricemia
Aggressive hydration
Rasburicase
Avoid nephrotoxic medications and hypotension
Indications for dialysis
Severe oliguria or anuria
Intractable fluid overload
Persistent hyperkalemia
Hyperphosphatemia-induced symptomatic hypocalcemia
Uric acid > 10 despite rasburicase
Disposition: ICU
TORCH Infections WITH Dr. Meigh
Have increased suspicion for these infections in mothers with no prenatal care
Commonly can see rash, lymphadenopathy, microcephaly, growth retardation, intellectual disability, sensorineural hearing loss
Toxoplasmosis
80% of mothers will be asymptomatic, 20% will have symptoms of a nonspecific viral illness
Neonatal presentation
Subclinical at birth in 70-90% of cases
Symptoms
Chorioretiniits
Intracranial calcifications
Hydrocephalus
Others: jaundice, hepatosplenomegaly, thrombocytopenia, lymphadenopathy, seizures
Treatment
Pyramethamine administered with leukovorin
Sulfadiazine
Treatment duration is for one year
Other - syphilis, VZV, parvovirus, Zika
Syphilis
Transmitted sexually with increasing incidence
Maternal presentation
Primary: chancre
Secondary: condyloma lata
Late syphilis: aortitis, gummatous lesions, tabes dorsalis
Treatment
Penicillin G 2.4 M units IM for primary and secondary disease
Tertiary disease requires three doses of IM penicillin G spaced at one week intervals
Neonatal presentation
Less than 2 years (early congenital syphilis)
60-90% asymptomatic at birth, symptoms will typically develop < 3 mo
Symptoms:
Syphilitic snuffles
Hepatomegaly
Maculopapular rash
CNS involvement
Long bone abnormalities with pseudoparalysis
Pneumonia
Greater than 2 years (late congenital syphilis)
May develop despite treatment
Frontal bossing or saddle nose
Hutchinson teeth
Sensorineural hearing loss
Saber shins
Treatment
10 days of IV penicillin G if symptomatic
If asymptomatic but born to high-risk mother can consider one-time dose of IM penicillin G
Rubella
Considered eliminated by the CDC
Transmitted via droplets
Maternal presentation
Viral illness: low grade fevers, cough, conjunctivitis, sore throat
Erythematous maculopapular rash spreading from face to trunk and extremities within hours
Forcheimer spots on the soft palate
Highest risk of congenital rubella syndrome at < 16 weeks gestation
Neonatal presentation
About 70% asymptomatic at birth
Congenital cataracts
Cardiac disease, most commonly PDA
Blueberry muffin rash
Deafness
Treatment is largely supportive
CMV
Most common congenital viral infection
Transmitted via close contact, sexual exposure, transfusion, organ transplant
Herpesvirus, so can reactivate and cause secondary infection
Maternal presentation: mononucleosis-like illness
Neonatal presentation
Only 10% symptomatic at birth
Sensorineural hearing loss
Petechiae
Microcephalus
Hepatosplenomegaly, juandice
Hypotonia, lethargy, seizures
Neurodevelopmental disabilities
Retinitis
Treatment
Mother: ganciclovir has not been shown to decrease transmission
Neonate: if symptomatic and less than 1 month old, valganciclovir or ganciclovir has been shown to have benefit
HSV
Maternal presentation
Prevalence of HSV-1 59%, HSV-2 21%
Primary infection: genital ulcers, dysuria, fever, adenopathy
Secondary infection: burning may precede other symptoms
Transmission typically during delivery, although transplacental and postnatal also possible
Treatment with acyclovir for 7-10 days for genital lesions, restart at 36 weeks until delivery
C-section recommend for active genital lesions or prodromal symptoms after rupture of membranes
Neonatal presentation
Skin, eye, and mouth: rash without organ involvement
CNS disease highest prevalence in first 2-3 weeks of life
Disseminated HSV typically presents within first week of life with multi-organ invovlement
Treatment: acyclovir, although duration depends on severity of disease
Pre-Hospital Sepsis Care WITH Dr. Spigner
Sepsis occurs more frequently in pre-hospital setting than stroke or STEMI, but is harder to diagnosis.
Septic patients that come to the ED by EMS have higher mortality.
Increased time to antibiotics leads to worse outcomes.
Prehospital qSOFA has been shown to have sensitivity of 42.9% and specificity of 93.8%.
Designing a Pre-Hospital Sepsis Screening Tool
SIRS more sensitive, qSOFA more specific
End-tidal CO2 is correlated with lactate and mortality in sepsis
EtCO2 performs better than any individual vital sign for predicting mortality
Screening tool of SIRS + EtCO2 < 25 mmHg produced PPV 78% and NPV 99%.
Southwest Ohio Sepsis Protocol
Inclusion age >16, suspect infection, >1 vital sign abnormality (SBP < 90, HR > 90, visible tachypnea, acute AMS)
Sepsis alert - EtCO2 < 25 and >2 abnormalities:
T > 100.4 or < 96
SBP < 90
HR > 90
RR > 20
AMS
Outcomes for studies of pre-hospital EMS screening
Lower times to IVF administration
Increased CMS core measure compliance
Lower time to IV antibiotic administration
No studies show mortality benefit
Pre-hospital Antibiotics
No difference in mortality between two groups although antibiotics were administered about 90 minutes earlier
Could be biased toward less severe sepsis patients
Demonstrates feasibility
74% admitted
5% BCx contamination rate
No adverse events
Podiatry WITH Dr. Henning
Lower Extremity Examination
Vascular
DP and PT pulses
Capillary refill time
Claudication
Doppler examination
Neuro
Numbness
Tingling
Burning
Skin
Ulcerations
Calluses
Signs of infection
Areas of pigment change
MSK
Focal muscle weakness
Structural abnormality
Joint range of motion
Vascular
Chronic Limb Threatening Ischemia
Ischemic rest pain with arterial insufficiency and gangrene
1 year amputation rate 12%
Arterial insufficiency can be characterized by foot redness that resolves with elevation
ABI Pitfalls
Can have false elevation secondary to calcification
Microvascular Thromboemboli (Blue Toe Syndrome)
Occlusive vasculopathy with arterial or venous thrombosis or emboli
Screen for atrial fibrillation, but most patients have had a recent vascular procedure
WIfI classification (Wound, Ischemia, foot Infection)
Grades from 0 (normal) to 3 (severe)
Classifies patient risk of amputation
Neurologic
Diabetic Neuropathy
Peripheral sensory and motor neuropathy with component of autonomic neuropathy
Can get tendon contractors along the flexor tendon that cause pressure ulcerations
Skin
Ulceration
Classic signs of infection: erythema, edema, malodor, drainage, warmth, or purulence
Obtain CT with contrast if concerned for abscess or necrotizing fasciitis
Weightbearing ulceration more common from neuropathic pressure ulceration
Often with surrounding callus
Ulcers in non-weightbearing areas are more commonly related to arterial, venous, or infectious etiologies
Necrotizing Soft Tissue Infections
Delay in diagnosis leads to increased morbidity and mortality
Diabetes is the most common comorbidity
Exam:
Hemorrhagic bullae
Crepitus
Pain out of proportion
Sepsis, shock
Puncture Wounds
Simple irrigation may be insignificant so have a low threshold for thorough incision and drainage
Consider prophylactic antibiotics, especially in patients with significant comorbidities or dirty wounds
Also consider drains or packing to leave wounds open so as to prevent abscess formation
Nail Bed Injuries
Includes lacerations, hematoma, avulsions, crush injuries
Be cautious of underling fractures
Musculoskeletal
Charcot Arthropathy
Pathologic process of osseous destruction, resorption, and consolidation resulting in deformity
Commonly in diabetic patients
About 20% have history of low energy trauma
Unclear pathophysiology
Often looks like a skin and soft tissue infection, although erythema will resolve with elevation unlike in infection
Treatment is casting and non-weight bearing
Gout
Most often affects 1st MTP, then midfoot and ankle
Keep a large differential
Lisfranc Injuries
Mechanism: axial load of a fixed foot, twisting, or crush injury
Look for plantar ecchymosis
If concerned and x-ray is negative, obtain CT scan or stress radiographs
Achilles Tendon Rupture
Edema, ecchymosis, palpable gap
Newer literature suggests nonoperative treatment if diagnosed early
Calcaneal Fractures
Classically these present after a fall from height
Be cautious for skin tenting - which can sometimes just present as blanched skin - as this can cause skin necrosis
Metatarsal Fractures
These are 35% of all foot fractures and usually result from a direct injury
Be cautious of skin tenting
Central metatarsals can tolerate displacement, but first metatarsal fractures typically have operative fixation due to weight bearing status
Quarterly Simulation: Inferior STEMI
Consider underlying medical etiologies for trauma with unclear etiologies like unexplained falls or single vehicle MVCs
Risk factors for high-degree AV block in STEMI:
RCA lesion
Greater than 65 years old
HTN
DM
Female
Two mechanisms for heart block in STEMI
Early: autonomic instability causes increased parasympathetic tone, which is generally responsive to atropine
Late: ischemia of the cardiac conduction system
Management:
Atropine
Pacing
Epinephrine
