Bronchiolitis

-2mo – 2 yo
RFs: < 1mo (prematurity of respiratory center), prematurity (<48w postconceptional age), chronic lung disease (bronchopulm dysplasia, tracheomalacia)*, cardiac disease, immunodeficiency, h/o apnea
-consider dispo to ICU for apnea monitoring and esp if pt has poor respiratory reserve at baseline (chronic lung/cardiac dz)
-ask re FH atopy/asthma and pt h/o eczema. Ask if prior wheezing.
O2 if sat <90%, nasal suctioning (esp if infant / obligate nasal) and O2 +/- trial bronchodilator – albut only (no atrovent). Only continue if positive response.
– RSV+ – higher risk of apnea
– if not severe (tachypnea, hypoxemia <90%, atelectesis or consolidation) or RFs, no labs or cxr
–if bil crackles/whz without URI symptoms, it’s not bronchiolitis! Consider CHF, FB
-there is variation in practice re whether or not to w/u for UTI in febrile pt >2mo with classic bronchiolitis symptoms
– no benefit of steroids or abx (unless high suspicion concomitant infection)
-HFNC at max 2 LPM/kg or bipap for wob. ivf for inability to tolerate feeds due to wob. consider inhaled epi, heliox with cpap.
-give palivizumab for pts <1yo with: hemodynamically significant heart disease or chronic lung disease of prematurity defined as preterm infants <32 weeks, 0 days’ gestation who require >21% oxygen for at least the first 28 days of life
-no need for RSV PCR testing unless diagnosis unclear or if pt in respiratory failure
ARDS salvage therapy: APRV and oscillator
-HFOV / oscillator = vibrating CPAP – TV 1-4mL/kg (very small) – maintains recruitment

Inhalational Injury

First Steps (stable pt)
-treat as a trauma pt (ABCDE) and look for traumatic injuries
-place pt on NRB with O2 to 15 L/m
—add nebs 4% lidocaine early to prepare for look at cords with video largynoscope
4:2:1 rule for burn pt fluid resuscitation
—start fluids even if no external burns visible, as pt will have insensible losses
-treat pain!

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Rule out
carbon monoxide toxicity: obtain serial blood gases (send co-oximetry) to monitor carboxyHb. Normal levels are 5 – 12%, depending on whether or not the pt is a smoker.
-cyanide toxicity: cyanide levels are not reliable in excluding toxicity, as it is rapidly cleared, and don’t result for days. Use lactate>8 or rising lactate despite fluid resuscitation to raise suspicion for toxicity
—ddx for elevated lactate (=impaired tissue oxygenation) in burn pt: cyanide, metHb, hypoxia, volume depletion
-look for rhabdo and AKI

Warning signs of respiratory failure
drooling or difficulty swallowing = impending failure
-monitor for stridor, hoarseness, and respiratory distress
-PaO2/FiO2 ratio indicates degree of pulmonary shunting past injured lung. PaO2/FiO2<300 forewarns respiratory failure

Intubation
-early elective intubation in a controlled setting is better than crash intubation of a pt with edematous airway structures
-Prepare multiple sizes ETTs in anticipation of vocal cord edema. Use the largest that will fit so that the pt can get a bronchoscopy upstairs. Prepare suction for soot-filled secretions. Sux is safe to use up to 24h post-burn.
-use volume controlled ARDS settings (6-8 mL/kg TV)
—airways and lung become less compliant in inhalational injury, so must prevent barotrauma and allow for permissive hypercapnea

****read NEJM paper****

Physiologically Difficult Intubation

Physiology
-when the pH or BP is low, optimize prior to giving sedative/paralytic and making the pt apneic
if you have time, check the blood gas, give fluid boluses, consider a bicarb push prior to intubation
-now is the time for push-dose epi! (NOT phenylephrine unless the pt is in afib RVR)

Oxygenation
-preoxygenate via nasal cannula + NRB each set to 15L/m, high flo, or BiPAP if underlying physiology dictates and pt can tolerate

O2 concentration in arterial blood:

CaO2 = (SaO2 x Hb x 1.34) + .003(PaO2)

Vertigo

Vertigo = sensation of self or room spinning (hallucination of motion)
-vs presyncope (lightheaded, faint)
-vs instability
-vs other (malaise, viral illness, anemia, depression)

Affected pathway:
3 sensory mechanisms (visual, proprioception, vestibular) –> vestibular nuclei in brainstem –> cerebellum

History: time and rate of onset, duration of symptoms
-change in mental status is red flag

Exam:
-nystagmus: downbeating, torsional, or nonfatiguable = central
-skew deviation (cover one eye):

Vertigo ALgorithm Rosens

CENTRAL CAUSES

Cerebellar Stroke
-red flags: sudden onset, occipital headache, severe gait ataxia…difficulty speaking
-risk factors: age, cardiovascular disease (HTN, CAD, smoking)

Cerebral Artery Dissection 
-carotid artery – anterior neck pain
-vertebral artery – posterior neck pain

Vertebrobasilar Insufficiency
one cause is subclavian steal syndrome
-check pulses and systolic BP in both arms

Acoustic Neuroma
-gradually progressive unilateral hearing loss and tinnitis
-vertigo rare!

 

PERIPHERAL CAUSES

BPPV
-normal at rest, onset with head movement

Vestibular Neuronitis
episodic, severe, lasting hours, symptom-free episodes

Meniere’s Disease
-vertigo, hearing loss, tinnitis

Labyrinthitis

Vestibulitis

 

 

Diffuse Abdo Pain

SBO
-simple obstruction
-closed loop obstruction = 2 points of obstruction (ex: 2 adhesions or a loop of bowel within a hernia sac) that prevent anterograde or retrograde flow of contents
—-rapidly progresses to ischemia and infarction
—-loop often twists on itself –> occludes large arteriesG
-can still have BMs with a complete SBO as residual stool is emptied

Pancreatitis
-exam may be impressive – may have acute abdomen
-3x nl lipase, peaks within 12-36h, NOT representative of severity
-if nl, consider early or acute-on-chronic –> CT
-fluid resuscitate! May need 10L/d
-abx (-penams) only for the sickest, ie severe sepsis or septic shock
-CT if diagnosis unclear or sick (eval for complication: necrotizing pancreatitis, pseudocyst)
-RUQ US to r/u surgical cause
-Complications: hypoCa, DKA, AKI, ARDS, pleural effusions, ?GIB

AAA
-elderly pt with new “renal colic” (back pain, hematuria), syncope + abdo pain, hip weakness/neuropathy (retroperitoneal rupture –> compression of femoral/obturator nerve)

Mesenteric Ischemia

ED Thoracotomy

West trauma guidelines
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-repair heart with 3-0 nonabsorbable running suture

Technique

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If hypotension persists following thoracotomy and pericardotomy, the descending thoracic aorta should be occluded to maximize coronary perfusion and to decrease the required effective circulating volume to facilitate resuscitation. Typically, the thoracic aorta is cross-clamped inferior to the left pulmonary hilum; alternatively, it can be clamped above the lung in the more proximal descending aorta. Blunt dissection with one’s thumb and fingertips can be performed to isolate the descending aorta. If the aorta cannot be easily isolated from the surrounding tissue, digitally occlude the aorta against the spine to effect aortic occlusion.

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After performing the thoracotomy and pericardotomy, the patient’s intrinsic cardiac activity is evaluated; patients in asystole without cardiac tamponade are declared dead.

Bimanual internal massage of the heart is initiated; this should be performed with a hinged clapping motion of the hands, with the wrists apposed, sequentially closing from palms to fingers. The ventricular compression proceeds from the cardiac apex to the base of the heart. Intracardiac injection of epinephrine may be administered into the left ventricle, using a specialized syringe, which resembles a spinal needle. Typically, the heart is lifted up slightly to expose the posterior left ventricle, and care is taken to avoid the circumflex coronary during injection. The heart is vigorously massaged to enhance coronary perfusion. After allowing time for vasopressors to circulate, the heart is defibrillated (30 J) using internal paddles. Following several minutes of such treatment, as well as generalized resuscitation, salvageability is reassessed; we define this as the patient’s ability to generate a systolic blood pressure of greater than 70 mm Hg with an aortic cross-clamp if necessary.

FYI
-Air embolism (West guidelines*): Treatment for bronchovenous air embolism demands immediate pulmonary hilar cross-clamping to prevent further propagation of pulmonary venous air. Placing the patient in the Trendelenburg’s position traps air in the apex of the left ventricle; then with an open pericardium, needle aspiration is performed to remove intracardiac air. In addition, aspiration of the aortic root may be required to alleviate any accumulated air. Vigorous cardiac massage may promote dissolution of air already present in the coronary arteries, and direct needle aspiration of the right coronary artery with a tuberculin syringe may be lifesaving. The production of air emboli is enhanced by the underlying physiology–there is relatively low intrinsic pulmonary venous pressure caused by associated hypovolemia and relatively high bronchoalveolar pressure from assisted positive-pressure ventilation. This combination increases the gradient for air transfer across bronchovenous channels. Although more often observed in penetrating trauma, a similar process may occur in patients with blunt lacerations of the lung parenchyma.

Sources:

*http://www.trauma.org/index.php/main/article/361/

*http://westerntrauma.org/documents/PublishedAlgorithms/WTACriticalDecisionsResuscitativeThoracotomy.pdf