Grand Rounds Recap 9.4.19

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MSK Ultrasound - QI/KT: hypothermia - Critical Care: shock - R4 Case Follow Up - R1 Clinical Diagnostics: HINTS EXAM - CPC: osteomyelitis

Musculoskeletal Ultrasound WITH DR. STOLZ

Shoulder

  • Normal anatomy

    • The glenoid and scapula should both be visualized at the level of the glenoid notch with the humeral head in the center of the screen

  • Shoulder dislocation

    • Ultrasound can be used in real time after a reduction as opposed to waiting for an x-ray

  • Shoulder effusion

    • Appears as hypoechoic material around the humeral head

  • Injection/arthrocentesis

    • Use an in plane technique and insert the needle laterally

  • AC joint assessment

    • Normal distance is 2-3 mm, and 6 mm is considered a separation

  • Biceps tendon pathology

    • Place the patient’s arm in a neutral position with the elbow flexed and palm facing up

    • Place the probe in the bicipital groove to look for the anisotropic tendon

Knee

  • Position the patient’s knee in slight flexion and use the linear probe

  • Scan from the terminus of the quadriceps tendon down to the insertion of the patellar tendon

  • The suprapatellar bursa is posterior to the quadriceps tendon and contiguous with the joint - this can be helpful to localize a pocket for arthrocentesis

Ankle

  • First obtain a longitudinal view on the anterior ankle to assess for an effusion between the distal tibia and talus.

  • Switch to a transverse view when performing an ankle arthrocentesis and approach from either a medial or lateral approach using an in plane technique

  • Finally, obtain longitudinal and transverse views on the posterior ankle to assess the Achilles tendon

    • Immediately anterior to the tendon is Kager’s fat and is useful for identifying the tendon

    • Posterior acoustic shadowing indicates a tendon rupture

QI/KT: Accidental Hypothermia WITH DRS. CONNELLY AND URBANOWICZ

Physiologic Changes in Hypothermia

  • Hypothermia initially causes vasoconstriction and atrial tachycardia, but eventually causes bradycardia and ventricular dysrrhythmias

  • Blood viscosity increases and coagulopathy develops at temperatures less than 32 degrees

  • Decreased cough and impaired ciliary function of the upper airways puts hypothermic patients at high risk for aspiration

  • Mental status changes begin at temperatures less than 32 degrees Celsius

  • As the patient gets colder, brain stem reflexes are lost and can mimic brain death

  • Hypothermia decreases ADH secretion and initially causes a cold diuresis which can causes significant hypovolemia

Severity of hypothermia

  • Mild - over 32 degrees

  • Moderate - 28-32 degrees

  • Severe - 24-28 degrees

  • Stability is classified primarily based on the patient’s mental status and vital signs

Rewarming Methods

  • Stable patients with mild hypothermia (32-35 degrees)

    • Passive external rewarming

      • Increase the ambient temperature of the room

      • Remove wet clothing to prevent further heat losses

      • Warm, sweet drinks - increases temperature 0.5-4 degrees per hour via shivering

      • Active movement - increases temperature 1-5 degrees per hour

  • Moderate hypothermia (28-32 degrees)

    • Active external rewarming

      • Chemical heat pack and blankets - use caution as these can cause thermal burns

      • Bair hugger - increases temperature by 1-3 degrees per hour

      • Arctic Sun - the evidence is scant for its use in the treatment of hypothermia and only at the level of case reports

    • Minimally invasive internal rewarming

      • Warmed IV fluids - studies showed no difference when compared with shivering alone, but recommended mainly because these patients are volume depleted and need crystalloid resuscitation

      • Warmed humidified oxygen - safe but does not significantly increase rewarming rate. This can cause airway injury when combined with positive pressure ventilation

      • Bladder irrigation - increases temperature by 0.5-1 degree per hour

  • Unstable or severe hypothermia (24-28 degrees)

    • Invasive internal rewarming

      • Endovascular rewarming

        • A central venous catheter is inserted and warm saline is infused into the device

        • Increases temperature by 0.5-2.5 degrees per hour

    • Extracorporeal rewarming

      • Continuous arteriovenous rewarming

        • Arterial and venous catheters remove the patient’s blood which is then warmed using a rapid infuser and placed back into the patient

      • Dialysis

        • Both CRRT and iHD have been used

        • Increases temperature by 1.5-3 degrees per hour

      • eCLS/ECMO

        • This method has the most robust amount of data with a 30% mortality difference and better neurologic outcomes

        • Increases temperature by 4-10 degrees/hr

        • Recommended in patients who have arrhythmias, SBP <90, respiratory distress, refractory acidosis, or temperature less than 28 degrees

  • Hypothermic arrest

    • ECMO

      • Small study of 13 patients showed significantly increased mortality rates

      • Contraindications:

        • Potassium greater than 12

        • Age greater than 70

        • Inability to be anticoagulated

        • Positive FAST exam

        • HOPE score < 0.10 (see below)

        • Core body temperature less than 14 degrees

    • Thoracic cavity lavage

      • Recommended if ECMO is not available

      • Highly variable rewarming rate - 1-21 degrees per hour

    • ACLS medications and defibrillation do not work well at low body temperatures - recommended to only administer 3 rounds until the patient is rewarmed, but CPR should be continued throughout

Outcome Predictions

  • Serum potassium

    • Elevated potassium suggests hypoxic death prior to hypothermia

    • If potassium is greater than 12, further resuscitative efforts should be terminated

  • HOPE Score

The hypothermia algorithm can be found on tamingthesru.com in the upcoming months!

Shock WITH DR. GORDER

Shock is a profound mismatch between oxygen supply and demand. Initially it is reversible but after a certain period of time becomes irreversible and leads to death.

Types of shock

  • Distributive

    • Sepsis - 62%

    • Other - 4%

      • Inflammatory shock

        • Appears similar to sepsis but no source is ever found (culture negative)

        • Severe burns, pancreatitis, air or fat embolism, aspiration

      • Anaphylaxis

      • Neurogenic shock

      • Endocrine shock

      • Drug or toxin induced (calcium channel and beta blocker overdose)

      • Liver failure

  • Cardiogenic - 16%

    • LV failure

      • Post MI

      • Acute valvular insufficiency

      • Cardiomyopathy

      • Dynamic LV outflow track obstruction

      • RV failure

        • Massive PE

        • Acute on chronic RV failure

        • Right sided MI

      • Cardiac contusion

      • Sepsis induced cardiomyopathy

  • Hypovolemic - 16%

    • Either hemorrhagic or non-hemorrhagic

  • Obstructive - 2%

    • Pulmonary embolism

    • Tension pneumothorax

    • Cardiac tamponade

    • Abdominal compartment syndrome

  • Patients may have as many types of shock as they please - don’t fall into the trap of only recognizing one type and anchoring on this

Recognition of Shock

  • Systolic blood pressure is representative of the patient’s cardiac output

    • Dependent on the stroke volume, which is in turn dependent on preload, afterload, and contractility

  • Diastolic blood pressure is representative of the systemic vascular resistance, or the overall vascular tone

    • Diastolic blood pressure will change first in distributive shock and cause a wide pulse pressure

  • Decreased blood pressure is the end pathway in shock, but patients in shock often initially present with normal blood pressure

  • No single test can diagnose shock - it is a bedside, clinical diagnosis

  • Start by assessing the patient’s hemodynamics

    • Look at the patient’s blood pressure in the context of their baseline - normotension may actually be hypotension in a patient with chronic hypertension

    • Tachycardia

      • Shock index - HR/SBP

        • Normal: 0.5-0.7

        • Several studies have shown that a shock index greater than 1.0 is associated with significantly poorer outcomes

      • Modified shock index - HR/MAP

        • Greater than 1.3 or less than 0.7 is a strong indicator for mortality

      • Tachycardia is the initial physiologic mechanism to increase cardiac output

        • At extreme rates (>200 bpm) diastolic filling decreases and leads to decreased stroke volume

        • Rate is usually not the problem - be very cautious with rate control or cardioversion in a tachycardic patient in shock

  • Low urine output

    • Every patient in shock should have a foley

    • Less than 0.5 cc/kg/hr is concerning for renal hypo-perfusion

  • Perfusion

    • Touch your patients - take their clothes off, put them in a gown, and look at and feel their legs - you can pick up cardiogenic shock if the patient’s legs are cold or have mottling

  • Altered mental status

    • Often profound in septic shock but a very late finding in cardiogenic shock

    • This is a harbinger of doom in hemorrhagic shock

    • Agitation is the last neuronal effort before death - do not take this away from the patient unless you are prepared to own their hemodynamics

  • Lactate

    • Classically taught as a marker of mismatch between oxygen delivery and demand - this is not true

      • No studies have shown a relationship between lactate and oxygen delivery

    • Lactate is a product of epinephrine-stimulated glycolysis - it is a result of aerobic metabolism, not anaerobic metabolism

    • The initial lactate can be useful in detecting occult shock, but trending lactate as a marker of resuscitation is not very helpful beyond for prognostics

    • Lactate is much more complicated than we realize, and we are probably not using it correctly

Diagnosis of Shock

  • History, physical, and chart review can rule out a vast majority of shock

    • Previous echo, cardiac cath, and EKG

    • Immunosuppression

    • Indwelling devices

    • Recent procedures

    • Recent medication changes

    • History of corticosteroid use

  • Ultrasound

    • RUSH Exam

      • This should be considered part of your physical exam for a patient in shock

      • Assesses cardiac function, valvular insufficiences, and can be a dynamic assessment when applying interventions

  • Invasive monitoring devices (Swan-Ganz catheter)

    • Have fallen out of favor

    • A PA catheter is only helpful if the patient is in truly undifferentiated shock or is in a mixed shock state

  • SvO2

    • In theory can tell you if the patient is in high or low output shock

    • There is a big difference in the SvO2 obtained from a central line and a Swan-Ganz

    • In the ED, the absolute number is unlikely to be helpful, but trends after interventions can be

  • Liver function testing

    • Remember to obtain these - you will often see more profound transaminitis in cardiogenic shock

R4 Case Follow Up WITH DR. BANNING

New onset seizure

  • Labs are abnormal in 15% of patients but only 1% contributed to making a final diagnosis

  • Imaging lead to a diagnosis in 10% of patients

  • Lumbar puncture aided diagnosis in 8% of patients

  • EKG - 14.2% of patients had some type of repolarization abnormality

Bigeminy

  • Can be causes by anxiety, sympathomimetics, myocardial ischemia, hyperthyroidism, hypokalemia and hypomagnesemia

Torsades des Pointes

  • Prolonged repolarization leads to T on P phenomenon, which then causes polymorphic ventricular tachycardia

  • The most common causes of torsades are QT prolonging medications

  • Treatment

    • 1-2 g of magnesium over 5-10 minutes

    • 100-200 J cardioversion or defibrillation

    • 1-1.5 mg/kg of lidocaine (preferred over procainamide or amiodarone)

R1 Clinical Diagnostics: The HINTS Exam WITH DR. IJAZ

Please see Dr. Ijaz’s fantastic post for more information on how to perform the HINTS exam, as well as examples of normal and abnormal findings and how to use the exam in your clinical practice in the ED.

Case 1: Vestibular neuritis

  • Treatment includes a trial of steroids, benzodiazepenes for vestibular suppression, and discharge with close PCP follow up

Case 2: Posterior Circulation Stroke

  • If you have a high clinical suspicion for a central cause of vertigo, the HINTS exam should not be used and the patient should proceed to definitive imaging / treatment

  • The NIHSS is often very low in posterior circulation strokes

  • Non contrast head CT has a poor sensitivity (unless a hemorrhagic stroke is identified)

    • You should obtain a CTA of the head and neck looking for basilar / PCA occlusion or vertebral dissection +/- a diffusion weighted MRI for non-LVO stroke

  • Treat this as a stroke with thrombolytics if the patient presents with neurologic deficits within the treatment window, and discuss with your local stroke team to determine if the patient should proceed to thrombectomy or other endovascular treatments

Case 3: Benign Paroxismal Positional Vertigo

  • The HINTS exam should not be used in cases of obvious BPPV - instead use the Dix-Hallpike maneuver

  • Treatment includes antihistamines such as meclizine or otolith repostioning maneuvers (Epley maneuver)

 CPC WITH DRS. FREDERICK AND SUMMERS

Case: A teenage male presents with right shoulder and left chest pain for the past week. The patient reports that he was bit by a bug and given keflex and developed the shoulder pain after this. The pain is reported as tearing and ripping in a dermatomal distribution on the left chest and right shoulder with associated vomiting and fevers. No PMH, PSH, known allergies, and he is fully immunized.

Physical exam: the patient is ill appearing with dry mucous membranes, tachycardic with a systolic murmur and delayed capillary refill. He is also tachycpneic with diminished breathe sounds over the left base. He has tenderness to palpation along the right biceps tendon and refuses to flex or abduct the right arm above 30 degrees.

He is given a fluid bolus, antibiotics, and tylenol and remains febrile and tachycardic.

His EKG shows sinus tachycardia. Laboratory studies show a potassium of 5.4, sodium of 135 and glucose of 110. He has no leukocytosis, mildly elevated imflammatory markers, normal urinalysis, and normal procalcitonin. He begins to desaturate to the high 80’s.

CXR and right shoulder x-ray are normal.

Bedside echocardiogram performed by cardiology appears hyperdynamic but otherwise is unremarkable. At this point a test is ordered and the diagnosis is made.

Differential Diagnosis

  • Distributive shock

    • Sepsis - osteomyelitis, septic arthritis, pneumonia, Lyme disease

    • Inflammatory shock

    • Endocrine shock - Addisonian crisis, pheochromocytoma, thyrotoxicosis

  • Cardiogenic

    • Lower on the differential given normal echocardiogram

  • Hypovolemic

    • Less likely with no history of GI losses

  • Obstructive shock

    • Pulmonary embolism is less likely in the pediatric population

    • No pneumothorax or effusion on chest x ray or echocardiogram

  • Infarction

    • Sickle cell disease

  • Glucose-6-phosphate dehydrogenase deficiency

  • Neoplasm

    • Osteosarcoma, ewing sarcoma, nephroblastoma/neuroblastoma with metastasis to lung or bone

  • Serum sickness like reaction to antibiotics

  • Autoimmunine

    • JRA, rheumatic fever, microscopic polyangitis, familial mediterranean fever, lupus

Test: MRI of the shoulder

Diagnosis: Acute hematogenous osteomyelitis of the proximal humerus

  • Osteomyelitis is twice as common in males

  • Risk factors include sickle cell anemia, immunodeficiency, and indwelling catheters

    • 1/2 of cases in pediatrics have no risk factors

  • Microbiogram: staphylococal sp., streptococcal sp., K. kingae, and E. coli

  • Presentation: constitutional symptoms with focal symptoms around the affected bone

  • Leukocytosis is only seen in about 36% of pediatric patients

  • ESR greater than 20 and CRP greater than 10 has a 95% sensitivity but are non-specific markers

  • X-rays appear normal until symptoms have been present for 10 days or longer

  • MRI is much more sensitive and specific than plain films

  • Treatment

    • Vancomycin for all patients

    • 3rd generation cephalosporin in patients less than 3 months of age

    • Treatment duration is a minimum of 4 weeks

    • Surgery is indicated if the bone damage is extensive or the patient does not respond to medical therapy