Grand Rounds Recap 4.27.22
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MORBIDITY AND MORTALITY CONFERENCE WITH DR. URBANOWICZ
Case 1: Pasteurella multocida
Household zoonoses:
Transmission from animals and primary human infection: Pasteurella species, Bartonella species, Capnocytophaga canimorsus, Toxoplasmosis gondii
Primary infection in animal and transmission to human: MDRO (E.coli, MRSA), Salmonella, Campylobacter, Cryptosporidium, Giardia, Rabies
Risk of infection with bites from the following species: dog 2-20%, cat 30-50%, human 10-20%
Factors that affect risk of infection: patient factors that affect immune response or healing such as obesity, age, and diabetes; whether wound incurred from a scratch or bite; time to presentation (>8-12 hours from time of injury have higher risk)
Cat teeth are narrower, and puncture wounds from their bites are associated with a higher risk of infection.
Crush or larger injuries requiring repair also carry a higher risk of infection
Hand and distal extremity wounds have the highest risk of infection followed by wounds involving vascular structure or prosthesis.
If antibiotics administered within 24 hours from injury, infection risk is 29.3% compared to 65% if within 48 hours and 81% if within 72 hours.
Pasteurella multocida is the most common infectious agent identified from common mammalian bites with rapid evolution of infection within 24-48 hours, bacteremia present in 25-50% of patients, high mortality around 25%, and antibiotic resistance to common antibiotics such as Cephalexin and Clindamycin.
Prophylactic antibiotics
A Cochrane Review updated in 2008 with 8 RCTs found no significant decrease in infection with prophylactic antibiotics administered for dog bites, cat bites or scratches, or based on the type of wound, but it did find a significant decrease in infection for human bites and with hand and foot injuries.
Potential best practices given advice from experts
Prescribe prophylactic antibiotics if:
Patient sustained injuries to hand, feet, joints, or face
Puncture wounds
Requires primary repair
Cat-related or deeper than epidermis
> 8 hours from time of injury
Age < 4 or > 65 yo
Any comorbidity which affects wound healing (DM, HIV, pregnancy, chemo, ESRD)
Management:
Irrigation ~ 250 cc per 1 cm
Antibiotic duration: 5-7 days with first dose in ED
Antibiotic choice: Amoxicillin-clavulanic Acid, Moxifloxacin, TMP-SMX or Ciprofloxacin or Cefuroxime PLUS Clindamycin or Metronidazole
Learning points:
Pasteurella is the leading cause of infection from mammalian bites and scratches
Cat-related injuries have significantly higher rates of infections than dogs
Antibiotic prophylaxis likely should be used in addition to extensive irrigation in some animal wounds, but not necessarily all
First line outpatient prophylactic agent is Amoxicillin-Clavulanic Acid
Case 2: Thyrotoxicosis
Mental health and substance use disorder account for a significant number of ED visits each year in the range of 12-22%. Many individuals in this syndemic of mental health and substance use may experience psychosis as part of their presentation.
According to 2018 study, of the 112,000 patient encounters for medical clearance studied, about 80% had at least ONE test ordered for medical clearance with the most common being CBC, a tox screen, or testing of BUN/Cr.
ACEP 2017 Policy supports minimal testing for medical clearance. “Routine or ancillary laboratory testing for psychiatric patients has little or not use in the ED.”
Caveats to the above may hinge on the following important history factors: timing of symptom onset (new presentation?), employment, housing, or environmental exposures, travel and pets, HIV and syphilis exposure risk, sleep patterns, drug, alcohol, and caffeine exposure, medication changes or additions, metabolic red flags, neuro red flags, fever, weight changes, family history, trauma, collateral information
Key red flag physical exam findings
Vital sign abnormalities
Lymphadenopathy or neck masses
Skin conditions
Gait
Speech patterns
Abnormal orientation
Learning points:
New onset psychosis warrants further evaluation for medical etiology.
Patients with known psychiatric disease presenting with psychotic symptoms do not routinely require labs or imaging unless sparked by H&P.
Evaluation of psychotic patients requires very thorough history, review of systems and exam.
Collateral information is priceless
Case 3: VP Shunt Complications
Hydrocephalus can be categorized as communicating (non-obstructive) or non-communicating (obstructive)
Communicating (non-obstructive): CSF interventricular flow is preserved, can occur with or without changes in CSF absorption. Common etiologies include NPH, meningitis. All ventricles will appear dilated on imaging.
Non-communicating (obstructive): CSF flow is impaired and is often caused by mass or mass effect from something like a catastrophic SAH. It is never associated with impaired CSF absorption.
Shunt dependence occurs in 75% of all cases of treated hydrocephalus and in 50% of children with communicating hydrocephalus. Shunt failure occurs in 4%of patients within 2 years and 98% failure within 10 years.
VP shunt anatomy and component parts
Components: proximal catheter positioned in frontal horn of either lateral ventricle; reservoir outside of the cranium, which samples CSF and measures intraventricular pressure; valve that regulates flow into the distal catheter; and distal catheter, which drains most commonly into the peritoneum or can also drain into the right atrium or pleural space.
Make sure to document skin exam related to any patient with a VP shunt.
VP shunt complications
Symptoms with the highest PPV for VPS complication include nausea, emesis, decreased level of consciousness, headache, lethargy
Common complications include obstruction, interruption, malpositioning, mechanical failure, over drainage, loculation development, infection
Obstruction can occur proximally and distally.
Interruptions may be detected on shunt series, which you should review for each of your patients.
Migration may occur as a patient grows when young or experiences significant weight gain when older.
Over drainage can lead to slit ventricle syndrome (collapse of ventricles into orifice of catheter resulting in occlusion). Depending on the rate of decompression, patients are at risk for SDH due to tearing of bridging veins.
VP shunt infection usually occurs within months of placement or revision and is associated with high morbidity. Causative agents often include skin flora. Definitive diagnosis made via shunt tap or LP. Cover empirically with both skin flora and GI flora coverage for VP shunts.
VP shunt diagnostics
Shunt series: +LR 80%, -LR 7-12%
CTH non-contrast: +LR 23-83%, -LR 9%
MRI: sensitivity 14-53%, specificity 99%
Learning points:
Hydrocephalus is a common both pediatric and adult disease
VP shunt malfunctions are common and present with nausea, vomiting and change in level of consciousness
Shunt series alone usually sufficient to evaluate for shunt integrity
Shunt infections require high clinical suspicion
VP shunt taps are to be completed by neurosurgery
Case 4: Guillain-Barré Syndrome (GBS)
Epidemiology
GBS is the most common cause of acute flaccid paralysis worldwide, estimated at 100,000/year. It is more common in men than in women and increases with age.
Even with treatment, mortality is around 5%, and 20% lose independent ambulatory function permanently.
Antecedent illness in ~75% of patients
Known causative organisms include: Campylobacter jejuni, Mycoplasma pneumoniae, HIV, Cytomegalovirus, Epstein-Barr Virus, Hepatitis E Virus, Varicella Zoster, Zika Virus, SARS-CoV-2
Presentation
Notably, only 25% of patients are diagnosed on their first visit.
Neuropathic pain localized to the thighs and low back is a common presenting symptom.
Symptoms progress until nadir 2-4 weeks after onset.
Dysautonomia (tachycardia most common) and shortness of breath are common.
Remember to document and monitor respiratory parameters for these patients: FVC/NIF/breath count - 20-30% of these patients will require intubation.
Diagnosis
This is a clinical diagnosis, but lumbar punctures typically performed and demonstrate albumin-cytological dissociation. MRI may also be helpful and could demonstrate cauda equina enhancement.
Greater likelihood of GBS with relative symmetry of symptoms, limb involvement at onset, muscular or radicular pain that is new onset, and cranial nerve involvement, especially bilateral facial palsy
Less likely to be GBS if persistent asymmetry, bowel or bladder involvement at onset, isolated respiratory dysfunction, hyperreflexia, or rapid progression in < 24 hrs
Scoring systems exist, but are not functionally helpful and again default to clinical judgment.
The clinical variant - Miller Fisher Syndrome - characterized by ophthalmoplegia, ataxia, and areflexia, occurs in approximately 5-10% of cases in the US and Europe and 20% of cases in Asia.
Management
No treatments to alter disease progression, though steroids, IVIG, and PLEX have all shown to improve time to recovery. There is no difference in the extent of disease at the nadir.
Recommend early physical therapy
Neurology consult in the ED
Learning points:
Guillain-Barré is the most common cause of acute flaccid paralysis worldwide and has high associated morbidity
Symptoms often begin as pain without weakness, are relatively symmetric, and progress over 2-4 weeks but are not necessarily ascending sensorimotor
Is a clinical diagnosis and requires high degree of suspicion
30% of patients will require intubation
Case 5: Ovarian torsion in pregnancy
Non-obstetric emergent surgeries occur in ~ 2% of patients with abdominal pain as the presenting complaint in 75% of these.
5x increased incidence compared to non-pregnant states, which increases further with ART. The highest risk occurs during the first trimester due to corpus luteum cysts, and the right ovary is most often affected.
Presentation
May find pain out of proportion on exam
Remember, a peritonitic abdomen is never normal, even in pregnancy. There are pregnancy-specific etiologies for abdominal pain such as round ligament pain, braxton-hicks, and normal uterine stretch, but these are typically mild, located near the pelvis, and are rarely severe. Do not forget your traditional differential for abdominal pain… appendicitis, cholangitis, obstruction, cholelithiasis, pancreatitis, etc.
Diagnosis and management
Doppler evaluation has a high false-negative rate (specific, but not sensitive). The ovary has dual blood supply and, therefore, can appear to have normal doppler flow on US, even in the setting of ovarian torsion.
May require surgery for definitive diagnosis
Obstetrics consultation
Learning points:
Non-obstetric abdominal emergencies are common and include appendicitis, cholelithiasis and small bowel obstruction
Ovarian torsion is 5x more common in pregnant patients with increasing incidence due to assisted reproductive technology
Dopplers have high false negative rates in evaluation for torsion
Clinical suspicion with low threshold for additional imaging, gynecology consultation or serial exams is often necessary to make these diagnosis
R1 CLINICAL DIAGNOSTICS: LYMPHEDEMA AND ITS MIMICS WITH DR. HAFFNER
Pathophysiology
Pathophysiology of lymphedema relates to hydrostatic pressure (pressure of blood pushing outward on the capillary and relatively small pressure of tissue fluid pushing back into the vessel) as well as oncotic pressure (created by solute mismatch across the permeable endothelial membrane).
The net direction of flow is the sum of these two types of pressures. There is generally greater net outflow than inflow with about 90% of filtered fluid reabsorbed.
The 10% of fluid remaining in the interstitium along with fat and proteins is where lymphatics come into play.
The lymphatic system is a separate low-pressure, unidirectional vascular network composed of more permeable vessels.
Presentation:
There is often a progression of exam findings from non-tender, pitting edema > dimpled peau d’orange texture > indurated, leathery texture > elephantiasis nostras verrucose.
Patients often experience discomfort or heaviness of the affected extremities.
Kaposi-Stemmer Sign - inability to pinch the fold of the second digit.
Edema is typically not detectable until interstitial volume is about 30% above normal.
According to one study of physical exam findings associated with lymphedema, only Kaposi-Stemmer sign has an OR of 7.88 predictive of lymphedema with a p value of 0.02. Non-pitting edema, square toes, and dorsal hump were not significantly predictive.
Etiologies:
Primary lymphedema
Hereditary lymphedema
Lymphedema Praecox
Lymphedema Tarda
Secondary lymphedema - typically acquired deficiencies to otherwise normally functioning lymphatic systems
Filariasis is the most common cause globally and is due to infection with Wuchereria bancrofti, which is endemic to parts of Asia, Africa, and the South Pacific. Lymphedema results from obstruction of lymphatics by adult worms with subsequent release of microfilariae into the blood as well as immune response to death of adult worm. Treat with Diethylcarbamazine, Ivermectin, and Albendazole.
Malignancy is the most common cause of lymphedema in the US and relates to direction obstruction of the lymphatic system by a tumor, lymphatic infiltration, or secondary to treatment. Breast cancer related lymphedema (BCRL) occurs in about 21% of individuals and average presentation is about 2 years after diagnosis or surgery.
Obesity - adipose deposition can also cause lymphatic obstruction, and lymphedema may be further worsened by decreased physical activity.
Acute adenolymphangitis (ADL) refers to sudden onset of fever and painful lymphadenopathy due to immune response to dying worms. May also get a secondary bacterial infection on top of this.
Additional diagnosis to consider:
Chronic venous insufficiency results from increased hydrostatic pressure, which can break down valves and cause damage to capillary basement membranes. This can also lead to tissue hypoperfusion and hypoxia, causing inflammation, atrophy, and ulcer formation occasionally. Varicosities and hyperpigmentation observed due to RBC breakdown and hemosiderin release. Management involves leg elevation to decrease hydrostatic pressure.
`DVT - thrombosis of deep vein in leg or pelvis, differentiated from lymphedema by rapid onset, risk factors. Consider using Well’s Criteria and low threshold to ultrasound.
Cellulitis - similarly differentiated by quick onset, warmth, erythema, and fever. Lymphedema is a risk factor for recurrent cellulitis.
Lipedema - chronic progressive disorder of bilateral lower extremities with subcutaneous accumulation of adipose tissue, presents in pubertal women. Foot sparing.
Myxedema - nonpitting edema due to deposition of glycosaminoglycans, associated with Graves’ Disease
Cardiac and renal failure
Diagnostic work up is essential to rule out other diagnoses, but should be targeted based on differential. It may include CBC, renal panel, LFTs, UA, lower extremity ultrasound, MRI (not sensitive or specific for lymphedema), lymphoscintigraphy (diagnostic tool of choice).
Management
Referral to PCP or specialist clinic
Prophylactic interventions and precautions
Skin care, regular hand washing, moisturize to avoid skin breakdown
Monitoring for signs of malignancy recurrence or secondary malignancies
Pharmacotherapy
No role for diuretics in lymphedema alone, but often prescribed for comorbid conditions
Some patients may be placed on prophylactic antibiotics (low dose Clindamycin)
Extremity elevation
Compression therapy - can result in 60% decrease in volume and is typically easier and cheaper than other treatments
Combined decongestive therapy - compression therapy, manual lymphatic drainage, exercise, and skin care
Surgical interventions reserved for refractory cases, either debulking or reconstructive approaches.
There are options in Cincinnati for specialized care at Drake, Cincinnati Children’s, Jewish Hospital, as well as TriHealth Rehabilitation and Physical Therapy Center
For more - see Dr. Haffner’s full post here
R2 CPC: HSV MENINGOENCEPHALITIS WITH DRS. STARK AND KOEHLER
Epidemiology and Pathophysiology
HSV is the second most common cause of viral meningitis and the most common cause of recurrent meningitis.
HSV is a common latent virus with about 90% of normal, healthy people being seropositive at any given time (despite the fact that only 25% of the population reports a history of either genital herpes or cold sores).
Prognosis: Mortality rate for HSV meningoencephalitis is much higher than most other aseptic encephalitis. Without treatment, mortality approaches 70%. Relapses are common.
HSV can be reactivated spontaneously or secondary to some trigger including trauma, sunlight, radiation, and immunosuppression. HSV meningoencephalitis can result from either latent virus reactivation or a primary herpes virus infection.
HSV is characterized as a necrotizing infection that is localized to the frontal and temporal lobes. This is thought to be secondary to entry of the virus via the olfactory pathway and spread along the base of the brain to the temporal lobes. Another theory is that HSV encephalitis is the result of reactivation from latent virus in the trigeminal ganglia, again with basilar spread to the temporal lobes.
HSV1 accounts for 90% of cases
Presentation
Typical symptoms include fever, headache, photophobia, meningismus, and confusion. One retrospective study found that 100% of patients complained of headache prior to presentation.
HSE specifically is also associated with frontal features including aphasia and personality changes or temporal features including seizures.
Exam is likely to be non-focal, though can have focal findings. May also observe fever, meningismus, progressive AMS, seizure activity, odd behaviors.
Workup
LP - Up to 5% of patients will have normal CSF, especially early in the disease course. LP may reveal a lymphocytic pleocytosis with increased protein and normal glucose. RBCs and xanthochromia are also common due to the necrotizing nature of the virus.
MRI is the most sensitive in detecting early lesions. Often CT is unremarkable during the first few days of symptoms. MRI may show evidence of edema and meningeal/viral enhancement in the frontal and temporal regions.
Focal findings on EEG are seen in over 50% of patients.
Treatment
Initiate as soon as possible given effect on morbidity and mortality
Acyclovir 10 mg/kg q8h
At least 14 days of treatment
Renal failure is common
R3 SMALL GROUPS WITH DRS. CHUKO, CRAWFORD, AND IJAZ
Transvenous pacing with Dr. Crawford
For our full post on the procedure see here
Indications for pacing: Hemodynamically unstable and symptomatic PLUS
Bradycardia
High degree AV nodal blockade
Drug overdose
Overdrive pacing (especially in the event of torsades)
Prepping for placement:
Site selection: RIJ > L SCV > L IJ > R SCV
Supplies: Pacemaker box and cables, TV pacer wire, adaptors, Cordis/MAC catheter, ultrasound, 2nd person to operate the box
Steps:
Place the Cordis or MAC introducer catheter in usual sterile fashion
Prepare the wire - (1) Insert adapters into the ends of the pacer wire (2) Test the balloon (3) Insert pacer wire into the sterile sheath
Connect and set up the box
Non-sterile assistant needed for this step.
Make sure that the cable is in the “V” port.
Connect the pacer wires to the generator box (+ to + and - to -). Of note, positive is sometimes labeled as proximal.
Turn box on > Switch pacer to “VVI” (ie, ventricular paced and sensed) > Set rate to 2x intrinsic rate > Turn atrial pacing to 0 > Turn ventricle to 20 mA > Sensitivity defaults to 2 mV
If you forget the above settings, press DOO, which triggers asynchronous pacing in atria and ventricle
Float the wire to a depth of 20 cm > inflate the balloon with 1.5 cc of air and lock > advance wire until you see a jump in HR and electrical capture on telemetry > evaluate for mechanical capture via pulse ox and femoral pulse on US > decrease mA until you lose mechanical captures and then increase by 1-2 > deflate the balloon. Remember to orient the ballono to the anticipated anatomic path throughout this step.
Secure the wire - Extend the sterile sheath, make sure that the line is stitched in place, hang the pacer box on an IV pole
Confirm placement - wire should cross midline, confirm with US, still need CXR though for line placement
