Grand Rounds Recap 4.13.22
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r4 case follow WITH dr. frederick
Massive Upper GI Bleed
A massive upper GI bleed can be defined in the following ways:
GI bleeding with a Hgb < 7
An abnormally elevated shock index
500cc of hematemesis in 24 hours
Any volume of hematemesis that makes an ED provider say “Oh boy that’s a lot of blood!”
Mimics of Massive GI bleed
Epistaxis - Massive epistaxis will demonstrate the nose as the source upon intubation if not sooner
Hemoptysis - Typically these patients have more significant respiratory compromise and the blood coming up will be bubbly/frothy and aerated.
Hematemesis (not a mimic) - Will frequently have dark brown appearance mixed in due to blood digested in stomach acid
Causes
Ulcers are responsible for 40-50% of cases, variceal bleeding 5-30% of cases, esophagitis about 10% of cases, vascular malformations about 5% of cases.
Stabilization
Control the airway
Give them blood
Proton pump inhibitors - only helps with bleeding related to ulcers, may not actually stop the bleeding but decreases the chance of re-bleeding / need for repeat EGD.
Octreotide - causes splanchnic vasoconstriction and may slow variceal bleeding.
TXA - NOT recommended. The HALT-IT trial demonstrates no benefit , but may increase VTE and seizures (when compared to placebo).
Esophageal tamponade tubes
Linton tube - only contains a gastric balloon
Blakemore tube - contains and esophageal and gastric balloon, but only a gastric aspiration port
Minnesota - contains an esophageal and gastric balloon, as well as gastric and esophageal aspiration ports (prevents blood from pooling into the esophagus and being aspirated into the airway).
Improve the course
Erythromycin - improves gastric emptying and allows improved visualization (and therefore intervention) on EGD. Try to give it about 30-90 minutes before EGD.
Ceftriaxone - decreases mortality from potential infection due to translocation of gut bacteria.
Clinicopathologic conference WITH Drs. kletsel and ham
Credit to Dr. Ham who crushed this CPC case and successfully came to the diagnosis of:
Cat Scratch disease (Bartonella Henselae infection)
Annual incidence of 4.7 per 100,000. Ohio has the 3rd highest incidence in the country.
The bacteria are carried by cats, most common in kittens, with about 90% of cats under the age of 1 yo being carriers.
Once humans are infected (by cat scratch or bite) they become the hosts of the disease.
The disease causes an acute inflammatory reaction within 3-10 days, resulting in a localized skin reaction and lymphadenopathy. This can progress to disseminated disease over the subsequent weeks. Disseminated disease results in visceral organ involvement and is most common in children. Disseminated disease results in fevers, abdominal pain, and weight loss. Central nervous system manifestations can include encephalopathy, transverse myelitis, and cerebellar ataxia. Ocular involvement manifests as neuro-retinitis which presents with optic nerve edema and acute or subacute vision loss.
Diagnosis is made by serology testing
Treatment
Regional lymphadenopathy and local skin reaction is treated with Azithromycin x 5 days or Bactrim x 7-10 days.
If hepatosplenic disease is present, The course of azithromycin is extended to 10-14 days and rifampin is added.
If neurologic or ocular symptoms are present, the course of rifampin is extended to 2-6 weeks and doxycycline is added for the same duration.
R1 Clinical Diagnostics: “Dysnatremias” WITH Dr. Chhabria
Hyponatremia
Severity
Mild 130-135
May have fatigue and cramping
Moderate 125-129
Nausea and Headaches
Severe < 125
Seizures or dysrhythmias
If the hyponatremia is chronically developing, even patients with severe hyponatremia may present with very mild symptoms.
Chronicity
Acute < 48 hours
Chronic > 48 Hours
Hypotonic hypovolemic hyponatremia
These patients are hypovolemic with hyperosmolarity
Can be caused by renal failure, adrenal crisis, cerebral salt wasting, and diuretics (especially thiazide diuretics)
Hypotonic euvolemic hyponatremia
Can be caused by renal failure, SIADH, glucocorticoid deficiency, or be exercise induced.
Can be treated with removal of the offending medication (if present), fluid restriction, and medications including Tolvaptan and Demeclocycline (not widely recommended presently).
Hypotonic Hypervolemic hyponatremia
Seen with renal failure which results in fluid retention as well as CHF and Cirrhosis. This results in a delusional hyponatremia.
Keep the patient NPO to limit fluid retention. Consider adding a loop diuretic to assist with excretion of excess volume. Vaptans (vasopressin antagonists) can also be utilized to induce diuresis.
Beware of overly rapid correction of hyponatremia (especially chronic hyponatremia) which can result in osmotic demyelination syndrome. For a deeper dive on this, check out Dr. Frederick’s Annals of B-pod article here!
If the patient presents with severe CNS dysfunction and seizures, treat rapidly with hypertonic as below:
Algorithm for treatment of hyponatremia
Hypernatremia
Severity
Mild 145-150
Moderate 150 -160
Severe > 160
Chronicity
Acute < 48 hours
Chronic > 48 Hours
Hypovolemic Hypernatremia
Can be seen with diuretics, GI losses, significant sweating, and dehydration.
There is an increased loss of free water which results in increased sodium concentration.
Oral or IV hydration is the mainstay of treatment, ideally with ½ NS or D5W. If the patient is so severely dehydrated as to have hemodynamic compromise, start their rehydration with isotonic fluids.
Algorithm for treatment of hypernatremia
r3 taming the sru WITH dr. Frankenfeld
Basilar Artery Occlusion
Accounts for 1-4% of all strokes and about 20% of posterior strokes
Has an incredibly high mortality that approaches 86% without treatment
May have a rapid onset but can also be stuttering, insidious, and have a prodromal period with micro-strokes heralding complete occlusion.
Signs and symptoms include vertigo, vision changes, ataxia, and loss of consciousness. On exam patients may have a dysconjugate gaze, pupillary defects, nystagmus, gait abnormalities, ataxia, and flexor posturing.
Posterior Stroke Syndromes
Wallenberg Syndrome - PICA Occlusion: Horner’s syndrome, dysarthria, dysphagia, ipsilateral face hemiparesis and contralateral body hemiparesis.
Pancioli Pearls: These patients may present with hiccups
Locked-in Syndrome - Mid Basilar Occlusion: Patients may appear obtunded, unresponsive and comatose, but should have preservation of their vertical gaze, and this may be the only clue that they are actually awake and alert
Tip of the Basilar Syndrome: Presents with behavioral changes such as hypersomnia, hallucinations, and a vertical gaze palsy
COVID and Clotting
Patients with COVID-19 infections have been shown to have a higher rate of stroke. Additionally, patients with COVID-19 associated strokes were more likely to have an LVO and a higher NIH than non-COVID-19 associated strokes.
Combined pediatrics lecture : Pediatrics broken bones WITH our CCHMC PEM Colleagues
PEdiatric bone regions
Salter Harris Fractures
S - Salter Harris I: Straight through the growth plate (5%)
A - Salter Harris II: Above the growth plate (75%)
L - Salter Harris III: beLow the growth plate
TE - Salter Harris IV: Through Everything
R - Salter Harris V: cRushed growth plate
Supracondylar Fracture
The most common elbow fracture in pediatric patients (60%)
Non-displaced fractures need to be placed in a posterior long arm splint and referred for outpatient orthopedics evaluation
Displaced fractures need to be transferred for orthopedics reduction and operative repair.
Radial head fractures
More common in patients > 5 yo
May cause referred wrist/hand pain but they typically have focal tenderness at the radial head.
Monteggia Fracture and Galeazzi fractures
Remember the mnemonic MUGR
Monteggia = Ulnar fracture, A is proximal, so the dislocation of the radius is proximal.
Galeazzi = Radial Fracture, Z is distal, so the dislocation of the ulna is distal
Buckle/Torus fracture of the forearm
Can be splinted with a premade wrist splint and follow up in ortho clinic as an outpatient.
Other Forearm Fractures
Patients over the age of 10 with more than 10 degrees of angulation need to be reduced
Patients under the age of 8 can tolerate up to 20-25% of flexion-extension angulation and 10 degrees of radial-ulnar deviation
Salter III, IV, and V or open fractures should all be transferred for orthopedic evaluation.
Seymour Fractures
A displaced distal phalanx physis fracture associated with a nail bed injury.
Accounts for about 20-30% of pediatric phalangeal fractures.
Treatment is antibiotics, and transfer for evaluation by orthopedics as this requires open reduction, washout, and pinning.
Tillaux Fracture
A Salter Harris III fracture of the anterolateral distal tibial diaphysis.
This requires reduction to <2mm of displacement. If you cannot achieve this reduction, this will require ORIF. Have a very low threshold to get a CT post manipulation to assure adequate reduction.
Triplane Fracture
A Salter Harris IV of the Tibia in multiple planes. Can have 2, 3, or 4 fracture parts.
Epiphysis is often fractured in the sagittal plane (seen on AP)
Physis fracture is appreciated in the axial plane
Posterior aspect of the metaphysis is fractured in the coronal plane (seen on lateral)
Results in the Mercedes Benz Sign on axial CT scan
Pelvic avulsion fracture
Typically seen with sports involving sprinting.
Management is usually conservative. Bed rest can be prescribed for severe pain, otherwise crutch-assisted weight bearing is appropriate until they are pain free. Pain can be managed with NSAIDs and Ice packs. Patients can be referred to outpatient orthopedics for physical therapy +/- surgery (depending on the distance of distraction of the avulsed bone).
