Any postpartum women presenting with persistent fever of >38.0C should be assumed to have a genital tract infection until proven otherwise. Other common sources of fever include respiratory tract infection, UTIs, mastitis, and thrombophlebitis. However, Pelvic infection is the most common serious complication of the puerperium. Risk factors of Postpartum Endometritis
Cesarean Section
Multiple Gestation
Younger maternal age
Prolonged labour and PROM
Internal fetal monitoring
Digital examination
Immunocompromised state
Common Bugs (reside in the bowel and colonize the perineum, vagina, and cervix)
Gram-positive and gram-negative aerobes, anaerobes
Chlamydia trachomatis, and Neisseria gonorrhoea
Gardnerella vaginalis is isolated more often in younger women.
MRSA
Many infections are polymicrobial
Clinical Presentation
Fever 38.0C
Foul-smelling loch
Leukocytosis
Tachycardia
Uterine tenderness
ED Management
ABC
General Sepsis Care (Fluids, Antibiotics, Cultures, Septic Screen). Combination of Ampicillin or Clindamycin plus gentamicin is sufficient for 90% of patients
Drainage of abscesses and purulent material or debridement of necrotic tissue
OBGYN Consultation
Complications of endometritis include parametrical spread of infection, pelvic abscesses; infected hematomas; septic pelvic thrombophlebitis; necrotizing fasciitis; and peritonitis.
Acute aortic dissection is part of a spectrum of diseases referred to as Acute Aortic Syndromes which basically encompasses 3 related conditions: (1) Aortic dissection (2) Intramural hematoma (lacks blood flow in the false lumen or its lack of an intimal flap or entry point. Believed to originate from a rupture of the vasa vasorum within the medial layer; or from microscopic intimal tears) (3) Penetrating atherosclerotic ulcer (typically seen in older population and often found incidentally, may progress to intramural hematoma)
The pathology, diagnosis, and treatment of these three entities are similar
Presentation While aortic dissection usually presents with severe
pain, its presentation can be more subtle and should
be considered in anyone with chest pain, back pain or abdominal pain and pain
with either syncope or focal neurological deficits. Aortic dissection can also present as an acute stroke. There are 2 main anatomic classification systems:
Stanford type B dissections are further classified as: 1. Complicated - Radiographic evidence of thoracic aortic rupture (eg, blood outside the aortic wall); ischemia involving the viscera, kidneys, spinal cord, or lower extremities; persistent pain; or rapid expansion in the distal arch or proximal descending aorta to a total aortic diameter of > 4.5 cm.These findings require immediate intervention due to the threat to life and limb. 2. Uncomplicated
The dissection creates a new false lumen, which separates the media from the
adventitia and can extend either anterograde or
retrograde involving the aortic root, arch, or any of
the main aortic branches. The false lumen may compress the
true lumen and compromise blood flow to distal
arteries and causing ischemic complications such as
renal failure, stroke, spinal infarction, limb ischemia,
and myocardial events. Classically, aortic dissection will present with abrupt chest or back pain, but about 5% of patients with an acute aortic dissection will have no pain.
Aortic dissection should always be considered in the differential diagnosis of patients with suspected acute coronary syndromes or pulmonary embolism.
Atypical presentations can also occur.
Syncope has been reported in up to about 20% of patients
Acute neurological deficits or coma occur in 30% of patients presenting with an acute type A dissection. Neurological findings can be associated with aortic dissections secondary to the extension of the dissection into the aortic branches. These branches can be occluded by either expansion of the false lumen occluding the true lumen or by emboli from an expanding thrombus. Deficits may occur from insults to the brain or spinal cord.
Patients may be hypertensive (49%), normo- tensive (35%) orhypotensive (8%), or in shock (8%).The presence of hypotension or shock is an ominous finding.
Blood pressure discrepancy can occur when a dissection extends into a branch of the aorta occluding the subclavian artery. A difference of 20 mm Hg between arms is considered positive and can be suggestive of an aortic dissection (this finding cannot be used to rule out dissection); however, 20% of the population will have a blood pressure differential without an aortic dissection.
A pulse deficit is defined as having weak or no pulse on the affected side.However, data from the IRAD database of 2538 patients founda pulse de cit or blood pressure differential in only 20% of patients.
An aortic dissection may extend retrograde and involve the aortic valve or coronary arteries. A diastolic murmur can be heard in about 1/3rd of patients with an aortic dissection and may represent severe aortic regurgitation but the presence of a diastolic murmur is neither sensi- tive nor specific for aortic dissection.
2-5% of patients with aortic dissections will have concurrent myocardial ischemia. Proximal aortic dissections can dissect into the right coronary artery, causing occlusion, and can present with a STEMI. If clinical suspicion for aortic dissection is present, other diagnostic modalities should be used to evaluate for proximal aortic dissection prior to anticoagulation or thrombolytics.
Cardiac surgery (eg, aortic
valve replacement, coronary artery bypass grafting) or percutaneous catheter placement (eg, cardiac catheterisation),
Diagnosis D-Dimer More and more evidence
is accumulating in support of the use of D-dimer as a
screening tool for aortic dissection but currently, only a few small studies have looked at
the sensitivity of D-dimer in ruling out aortic dissection (need further validation). Also, Intramural hematoma
or aortic dissections with a thrombosed false
lumen can have a false negative D-dimer. If
there is sufficient clinical suspicion for an acute
aortic dissection, advanced imaging is indicated.
A Negative D-dimer cannot rule out Aortic Dissection
Imaging Modalities for Acute Aortic Syndrome
CXR Chest radiography can suggest an aortic dissection. Abnormalities are seen in approxi- lately about 88% of patients.A widened
mediastinum is commonly associated with aortic
dissection and is seen in approximately 60% of patients.
A normal CXR cannot rule out
an aortic dissection.
Treatment
ABCs
Adequate Pain Relief (Morphine or Fentanyl)
Target HR< 60 beats/min and Target SBP between 100-120
mm Hg. Always start with Beta Blockers first (not vasodilators)
In case of cocaine toxicity, use benzodiazepines to decrease the sympathetic drive.
Type and Screen
If hypotensive with poor perfusion then use inotropes (can potentially worsen dissection due to increase in shearing forces) or consider pericardicentesis in cases of tamponade (poor prognosis)
Emergent Vascular Surgery Consultation - Type A acute aortic dissections require prompt surgical treatment. Definitive treatment of type B acute aortic dissections is unclear. Uncomplicated distal dissections have traditionally been treated with blood pressure control.Surgery has been reserved for patients who have persistent pain, uncontrolled hypertension, occlusion of a major arterial trunk, frank aortic leaking or rupture, or development of a localized aneurysm.
Rationale for Beta-Blockers First: Aortic wall stress is directly affected by the velocity of ventricular contraction over time (dP/dt). Initiation of treatment to decrease these shear forces should occur as soon as the diagnosis is made or suspected.intravenous narcotics
should also be given and titrated to pain control. Beta-blocker therapy should be given prior to initiating intravenous vasodilators to prevent reflex tachycardia. However, in cases of severe aortic regurgitation, use of intravenous beta
blockers or calcium-channel blockers with caution. Chronic Dissection Patients who present with chronic aortic dissection have already survived their period of greatest mortality risk and are usually treated by blood pressure control and close monitoring unless complications mandate surgery. All patients who have sustained and survived an aortic dissection, regardless of the type of definitive therapy used, require careful long-term surveillance and treatment.
Documentation:
Document HPI with pertinent negative findings
Presence of Absence of risk factors
Listen for bruits
Pulsate Mass, BP difference in lies or any pulse deficits
Neuro Exam and CXR, ECHO findings
Take Home
Use your gestalt to work up dissections. Read more here on ADvISED Trial. Currently, no validated clinical
decision rule exists to rule out an acute aortic
dissection. Historical and physical exam can be used to increase or decrease probability,
but atypical presentations are common.
Aortic dissection should always
be in the differential for patients with chest pain,
back pain, or abdominal pain.
Once the diagnosis is made or strongly suspected, ED Management is limited to pain relief, HTN and BP control and urgent Vascular surgery consulnation.
D-dimer and CXR alone should not be used to “rule out” aortic dissection. POCUS can be helpful in unstable patients but it should not be relied upon to
rule out an aortic dissection.
References and Further Reading:
Friado FJ. Aortic dissection: a 250-year perspective. Tex Heart
Inst J. 2011;38(6):694-700. (Review)
Hagan PG, Nienaber CA, Isselbacher EM, et al. The Inter-
national Registry of Acute Aortic Dissection (IRAD): new
insights into an old disease. JAMA. 2000;283(7):897-903.
(Retrospective; 464 patients)
2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/
STS/SVM guidelines for the diagnosis and management of
patients with thoracic aortic disease: a report of the Ameri-
can College of Cardiology Foundation/American Heart
Association Task Force on Practice Guidelines, American As-
sociation for Thoracic Surgery, American College of Radiol-
ogy, American Stroke Association, Society of Cardiovascular
Anesthesiologists, Society for Cardiovascular Angiography
and Interventions, Society of Interventional Radiology, Soci-
ety of Thoracic Surgeons, and Society for Vascular Medicine.
Circulation. 2010;121(13):1544-1579. (Guideline)
Mancini MC. Aortic dissection. Medscape. Available at: http://emedicine.medscape.com/article/2062452-overview.
Accessed June 10, 2013. (Review)
Hardie AD, Wineman RW, Nandalur KR. The natural his-
tory of acute non-traumatic aortic diseases. Emerg Radiol.
2009;16(2):87-95. (Review)
Collins JS, Evangelista A, Nienaber CA, et al. Differences in
clinical presentation, management, and outcomes of acute
type A aortic dissection in patients with and without previ-
ous cardiac surgery. Circulation. 2004;110(11 suppl 1):II237-
II242. (Retrospective; 617 patients)
Bossone E, Rampoldi V, Nienaber CA, et al. Usefulness of pulse de cit to predict inhospital complications and mortal-
ity in patients with acute type A aortic dissection. Am J
Cardiol. 2002;89(7):851-855. (Retrospective; 513 patients)
Rogers AM, Hermann LK, Booher AM, et al. Sensitivity of
the aortic dissection detection risk score, a novel guideline-
based tool for identi cation of acute aortic dissection at
initial presentation: results from the international registry of
acute aortic dissection. Circulation. 2011;123(20):2213-2218.
Lo BM. An evidence-based approach to acute aortic syndromes. Emergency medicine practice. 2013 Dec 1;15(12):1-23.
Presence of qRBBB in the setting of acute coronary syndrome signifiesproximal occlusion of left descending coronary artery with compromise of circulation in the septal arteries supplying the bundle branches. Anterior STEMi with RBBB is associated with a higher risk of death when compared with that of patients with normal conduction.
qRBBB with LAFBInstead of the rSR pattern (seen in RBBB), there is qRBBB pattern in V1 because the initial r wave has been knocked off by anterior wall myocardial infarction.
Due to anterior location of the right ventricle than that of the left ventricle, activation of the right ventricular free wall can neutralize the abnormal septal forces associated with an anteroseptal MI. Therefore, in most patients with an anteroseptal infarction, abnormal Q waves in right precordial leads is mostly manifest during RBBB showing the classical qRBBB pattern, due to delayed activation of the right ventricle.
Understanding RBBB RBBB causes delayed depolarisation of right Ventricle as depolarisation spreads across the septum (instead of the Right Bundle) taking longer than usual. This produces characteristic ECG changes described below in the diagnostic criteria. Left Ventricle depolarisation remains normal i.e normal early part of QRS complex.
Diagnostic Criteria
Broad
QRS > 120 ms
RSR’
pattern in V1-3 (‘M-shaped’ QRS complex) or a broad monophonic r wave or a qR
complex
Wide,
slurred S wave in the lateral leads (I, aVL, V5-6
RBBB
often shows STD and TWI in V1-3 due to secondary depolarisation
abnormalities
Causes
Ischemic
Heat Disease
Acute Pulmonary HTN (PE)
Chronic Pulmonary HTN (Cor Pulmonale)
Valvular
Heart Disease
Myocarditis
Degenerative
Diseases of conduction system
Congenital Heart
Disease
Overdose of Na Channel Blockers
Idiopathic
Transient and
Rate Related
RBBB should NOT have any ST
Elevation. Look for the qRBBB pattern and RBBB with LAFB (Leftward Axis, qR in
lead I, aVL, rS in lead III) pattern.
qRBBB in V1-4 with STE (Image from TheECGinAcuteMI)
Take Home:
Remember the qRBBB pattern morphology
RBBB should never have any ST elevation
When
in doubt, do serial ECGs and screening bedside ECHO to look for RWMA
References and Further Reading:
Mishra, V., Sinha, S. K., & Razi, M. (2016). Right
Bundle Branch Block: A Masquerader in Acute Coronary Syndrome. North American
Journal of Medical Sciences, 8(2), 121–122. http://doi.org/10.4103/1947-2714.177347
2. Widimsky P, Rohác F, Stásek J, Kala P, Rokyta R, Kuzmanov B, et al. Primary angioplasty in acute myocardial infarction with right bundle branch block: Should new onset right bundle branch block be added to future guidelines as an indication for reperfusion therapy? Eur Heart J. 2012;33:86–95.
Ganesan S, Kannan K, Victor A, Selvan KT, Arun R,
Majella JC, Kumar RS, Aravind A, Viswanathan N, District V. QRBBB in acute
coronary syndrome: Does it matter in modern era? Angiographic correlation.
Indian Heart Journal. 2015 Dec 1;67:S38.
Wong
CK, Stewart RA, Gao W, French JK, Raffel C, White HD. Prognostic
differences between different types of bundle branch block during the
early phase of acute myocardial infarction: Insights from the Hirulog and
Early Reperfusion or Occlusion (HERO)-2 trial. Eur Heart
J. 2006;27:21–8.
Viral Laryngotracheobronchitis (Croup) is the most common cause of
stridor commonly affecting children between 6 months to 6 years old, with a peak in the fall and early winter months. Croup is acquired through
inhalation of the virus.
Possible agents could be parainfluenza
virus (most common), rhinovirus. enterovirus, respiratory syncytial
virus, influenza virus and human metapneumovirus.
Clinical Presentation Typically, symptoms begin after 1
to 3 days of URTI symptoms (nasal congestion, rhinorrhea, cough, and low-grade fever). Classic symptoms include a harsh barking cough, hoarse voice, and stridor.
Symptoms often tend to be worse at night and the severity of symptoms is related to
the amount of edema and inflammation of the airway.
Diagnosis and Assessment of Severity Look for tachypnea, stridor at rest, nasal flaring, retractions, lethargy or agitation, and oxygen desaturation. Symptoms are most severe on 3rd or 4th day of illness. Agitation and crying increase oxygen demand and may worsen airway compromise. Bloods and imaging are only required in children who fail to respond to conventional therapy. X Rays may demonstrate “steeple sign” (subglottic narrowing).
Steeple Sign
Croup is a clinical diagnosis
Steeple sign may be present
in normal children and can be absent in up to half of those with croup
Management Treatment is directed at decreasing airway obstruction and keeping the child comfortable
Corticosteroids: All patients with croup get steroids as a one- time dose (PO/IM/IV). Steroids reduce the severity and duration of symptoms and result in a decrease in return visits and hospital length of stay. The long half-life of dexamethasone (36-54 h) often allows for a single injection. Studies have shown that dexamethasone dosed at 0.15 mg/kg is as effective as 0.3 mg/kg or 0.6 mg/kg (with a maximum daily dose of 10 mg). Effects can be seen within 1 hour of oral administration.Nebulized budesonide 2 mg as a single dose and IM dexamethasone (0.6mg/kg) are alternatives to PO dexamethasone in children who are vomiting.
Treatment of croup: Nebulized epinephrine for moderate to
severe croup and corticosteroids for all
Epinephrine: Epinephrine comes as two different forms: racemic, which is composed of
equal parts of L- and D-isomers, and L-epinephrine,
which is the drug routinely used in acute situations
in concentrations of 1:1000 and 1:10,000.
L-Epinephrine (1:1000): 0.5 ml/kg neb or 5ml maximum
Racemic Epinephrine (2.25%): 0.05ml/kg neb or max 0.5ml
Mild croup generally does not require epinephrine. For those
with moderate or severe croup who receive nebulized epinephrine,
observe in the ED for at least 3 hours before considering discharge. Epinephrine decreases airway edema through vasoconstrictive alpha
effects and acts wishing 10-min lasting up to 2 hours. The use of Adrenaline decreases the number of
children with croup requiring intubation, ITU admissions, and
admission to the hospital.
Observation for about 3 hours is recommended because an
increase in croup scores can occur between doses of epinephrine nebulisation
Intubation is reserved for cases of severe croup not responding to medical treatment. When intubation is necessary, use endotracheal tubes smaller than recommended for patient size and age to avoid traumatizing the inflamed mucosa.
Treatment options with limited evidence:
Cool Mist: Humidified air was used to treat croup, but they are no longer recommended as studies have consistently failed to show clinical improvement with these interventions.
Heliox (70% helium/30%
oxygen): Despite its theoretical benefits, studies show
no definitive advantage of heliox over conventional treatment.24-28
Beta 2 Agonists: Insufficient data. Concerns about risk of worsening upper airway obstruction asβ-receptors on the vasculature cause vasodilation (as compared to the
vasoconstrictive α effects of epinephrine), which might worsen upper
airway edema in croup, and there is no smooth muscle in the upper
airway. Therefore, β-agonists are not recommended for treatment
of croup.
Antibiotics have no role in uncomplicated croup
Antitussives have no proven effect on the course or severity of croup and may increase sedation
Differential Diagnosis (Consider if no relief with Rx)
Bacterial tracheitis
Laryngomalacia
Tracheomalacia
Vascular rings
Epiglottitis (unlikely if vaccinated)
Foreign body aspiration
Peritonsillar abscess
Retropharyngeal abscess
Tracheo-esophageal fistula
Admit
Moderate to Severe Croup
Looking toxic and not tolerating oral fluids
Comorbidities
Social Issues
Persistent
stridor at rest, tachypnea, retractions, and hypoxia
Discharge Advice
Advise the parents/carers to use either paracetamol or ibuprofen to treat a child who is distressed due to fever.
Encourage the child to take fluids regularly.
To check on the child regularly, including through the night.
Russell KF, Liang Y, O’Gorman K, Johnson DW, Klassen TP. Glucocorticoids for croup. Cochrane Database of Systematic Reviews 2011, Issue 1. Art. No.: CD001955.
Johnson DW. Croup. BMJ Clin Evid. 2009; 2009: 0321.
Bjornson, C.L. and and Johnson, D.W. (2013) Croup in children.CMAJ.185(15), 1317-1323
38.0C 
