Paediatric Gastroenteritis Review

Acute Gastroenteritis (AGE) kills thousands of children each year and consequences are worse in the developing world as diarrhoeal diseases occur on top of pre-existing malnutrition. It remains one of the most common ED presentation among children. Fortunately, most cases of acute gastroenteritis require minimal intervention, but severe dehydration and hypoglycemia may develop in cases of prolonged vomiting and diarrhoea requiring prompt management. The mainstay of treatment for mild-to-moderately dehydrated patients with acute gastroenteritis is oral rehydration solution (ORS). Antiemetics such as Ondansetron can decrease the need for intravenous fluids and hospitalisations.

Viral pathogens are the most common cause of AGE, accounting for up to 80% of cases

Common Bugs

E coli and Shigella are the most common bacterial pathogens in developing countries whereas Campylobacter is the most common bug in the developed world. Since most cases are viral, antibiotics are not required and only a few bacterial infections require treatment with antibiotics to hasten recovery and decrease bacterial shedding. It is critical to remember that some bacterial causes of colitis (ie, E coli O157:H7) can cause HUS that may be exacerbated by antibiotic administration. Therefore, antibiotics should not be started in most cases of suspected bacterial AGE until the species has been identified. Exceptions are made for children who are critically ill. Antibiotics do not come without side effects. Also, each course of antibiotics alters gut biome and can lead to a myriad of GI distress manifesting as abdominal pain, nausea, vomiting, and diarrhoea and  C diff colitis. Thus it is imperative to check recent antibiotic use in all patients who present with vomiting and diarrhoea. 

Children aged < 12 months should always be approached with a very broad differential. The most serious diagnosis to consider is intestinal malrotation and volvulus 

Brief Pathophysiology
Infection leads to gut biome alteration and host’s own immune system leads to inflammation of the lining of the stomach and intestines causing abdominal pain, nausea, vomiting, diarrhea, and hematochezia.

Vomiting that has continued for more than 24 to 48 hours without diarrhea is not AGE, and, while it may represent merely gastritis, a broad differential should be considered.

Key Questions in history:

• Color of both the emesis and stool (bilious or bloody emesis and bloody stools) 
• Fever
• History of recent travel and sick contacts 
• Quantity of urine output
• Regular medications or recent Antibiotic intake 

Protein allergies should be in the differential diagnosis in young infants presenting with vomiting and diarrhoea. 

Physical Exam and determining the degree of dehydration

• Vital Signs including CRT
• Hypotension is a late finding in children
• Segregate as  mild dehydration (< 3% loss of body weight - Normal exam), moderate dehydration (3%-9% loss of body weight - may have slightly sunken eyes, decreased tears, dry mouth, and slightly increased heart rate) or severe dehydration (> 9% loss of body weight - lethargic and tachycardic, with no tears, very dry mouth, and prolonged capillary refill)
• Abdo exam - localised tenderness to palpation. AGE might cause mild diffuse abdominal pain but not focal tenderness. 

Bloods, Imaging and Cultures

• Bloods are not required in mild to moderate illness. Inflammatory markers such as CRP has not been shown to differentiate viral versus bacterial causes of AGE and is not recommended in obvious cases of AGE. 
• Stool cultures and other stool studies are not required in most cases of uncomplicated AGE. However, in children with prolonged (> 3 days) or bloody diarrhea, toxic-appearance, and those with h/o recently travel abroad, stool cultures may be appropriate. 
• Stool ova and parasite examinations (Giardiasis, Toxocariasis and Cysticercosis)  are low-yield tests and should only be sent with appropriate travel history or prolonged disease with negative prior stool cultures or if there is evidence of weight loss or failure to thrive.
• Fecal calprotectin is an inflammatory marker in the stool which may aid in differentiating viral from bacterial AGE. Children with bacterial infections had signicantly higher levels of fecal calprotectin in the stool than children with viral infections. In general, fecal calprotectin does not affect the acute management of vomiting and diarrhea in the ED but it may be helpful in the outpatient workup of other illnesses, and can be sent in consultation with pediatric gastroenterology. 

Laboratory studies should be obtained in

all neonates with any level of dehydration and in

patients with an altered mental status not explained

by their suspected level of dehydration.

Treatment 

1. ABC (IV Cannula and fluid resus in critically ill, hypotensive, Consider Abx)

2. Antiemetics

PO/IV Ondansetron is safe and effective for AGE treatment in the ED. Vomiting children who are given ondansetron prior to an oral challenge are less likely to fail oral rehydration, require IV hydration, and be admitted to the hospital. Children treated with ondansetron also leave the ED sooner than those who are not given ondansetron prior to oral challenge. Most studies recommend the following oral pediatric dosing guidelines for ondansetron: children weighing < 15 kg: 2 mg; children weighing 15 kg to 30 kg: 4 mg; children weighing ≥ 30 kg: 8 mg. If the oral disintegrating tablets or oral solution are not available or tolerated, the IV preparation can be given orally. For children with severe dehydration in whom IV hydration will be started immediately, IV ondansetron can be given (0.15 mg/kg, max 8 mg).

3. Rehydration 

Liquids such as water, juices, sports drinks, soups, etc, are not traditionally recommended for mild-to- moderate dehydration because they do not contain the ideal ratio of sugars and salts to promote intestinal absorption, and they may serve as an osmotic diuretic. However, in a recent study from Canada, children with minimal dehydration due to AGE were treated with dilute apple juice had less treatment failure and less IV fluid administration. 

Oral challenge should be given as 5- 10 mL every 5 minutes for the first 30 minutes. If the child is tolerating, then the amount consumed can be increased by 5-mL increments over the next 30 minutes. Depending on the degree of dehydration, 50 to 100 mL/kg of ORS should be given over 3 to 4 hours to correct dehydration. Those who fail oral rehydration after antiemetics get IV (do Renal Function, Electrolutes, Glucose when inserting IV) or NG fluids. 

Majority agrees on starting with a 20 mL/kg NS bolus crystalloids. In children with stable blood pressure and normal capillary refill, infusion over 30 to 60 minutes is appropriate. In severely dehydrated patients appearing toxic, administer bolus IV fluids. Additionally, in if they are hypoglycaemic, then start with a 20 mL/kg bolus of D5NS followed by crystalloids. 

4. Anti-Diarrheal agents 
Loperamide is an opioid receptor agonist that acts as both an antisecretory and antimotility agents but has the potential of causing drowsiness and ileum. Thus it is strongly discouraged in children of all ages. Bismuth Salicylate is another option but it may cause salicylate toxicity if it is used incorrectly and therefore, it is also not recommended for use in children. 

Racecadotril is another antidiarrheal drug that has been shown in a few studies to reduce the duration and frequency of diarrhea in infants and children. It is an enkephalinase inhibitor and results in decreased secretion of water and electrolytes into the intestines. A recent meta-analysis of studies that examined the effectiveness of racecadotril in decreasing diarrhea found that it was well-tolerated and resulted in decreased duration of symptoms, as well as less stool frequency and volume. However, the included studies were of poor quality and subject to bias. 

  

5. Probiotics

• Probiotics are nonpathogenic organisms that work by regulating the gut biome and help to lessen in ammatory pathways. These agents help to decrease stool volume and frequency in AGE. Numerous studies have shown that Lactobacillus rhamnosus GG and Saccharomyces boulardii can reduce the length of diarrheal symptoms in children, with very few side effects but probiotics are probably most effective if started early. Also probiotics seem to have the greatest impact on diarrhea due to viral causes.
• Prebiotics are food products that promote the growth and activity of bacteria that reside in the gut and Synbiotics are a combination of probiotics and probiotics. 

6. Zinc

Zinc supplementation should be strongly considered when treating diarrhea in children residing in developing countries; supplementation significantly reduces diarrhea duration in children with underlying zinc deficiency. 


Safety Netting and discharge advise: Advise parents and carers of children:

• To continue usual feeds, including breast or other milk feeds and include ORS solution as supplemental fluid
• To discourage the drinking of fruit juices and carbonated drinks
• A rough calculation of the amount of ORS needed to replace emesis and diarrhea is 10 mL/kg for each episode of emesis or diarrhoea
• To seek advice if the child refuses to drink the ORS solution or vomits persistently
• Usual duration of diarrhoea is 5–7 days and in most children it stops within 2 weeks
• Usual duration of vomiting is 1 or 2 days and in most children it stops within 3 days
• Advise regarding hand Hygiene and inform that children should not go back to their school or other childcare facility until at least 48 hours after the last episode of diarrhoea or vomiting. 

Take Home:

• Start ondansetron early to children presenting with AGE. 
• Mainstay of treatment is oral rehydration with ORS and IV fluids are indicated only in severe dehydration or in children who are unable to take ORS orally.
• Laboratory studies are not indicated in mild-to-moderate dehydration due to AGE. In children with severe dehydration, start IV fluids and do renal function, blood glucose and electrolytes. 
• Probiotics can help decrease the duration of their diarrhea by approximately 24 hours but should be prescribed for children with AGE early in the course of their illness.Viral infections are the most common cause of AGE, so stool cultures are not needed. 

References and Further Reading:

1. http://pedemmorsels.com/diarrhea-and-dehydration/
2. http://pedemmorsels.com/probiotics-for-age/
3. Roslund G, Hepps TS, McQuillen KK. The role of oral ondansetron in children with vomiting as a result of acute gastritis/gastroenteritis who have failed oral rehydration therapy: a randomized controlled trial. Ann Emerg Med. 2008;52(1):22-29. 
4. O’Ryan M, Lucero Y, O’Ryan-Soriano MA, et al. An update on management of severe acute infectious gastroenteritis in children. Expert Rev Anti Infect Ther. 2010;8(6):671-682. 
5. Bonadio WA. Acute infectious enteritis in children. Emer- gency department diagnosis and management. Emerg Med Clin North Am. 1995;13(2):457-472.
6. Bruzzese E, Lo Vecchio A, Guarino A. Hospital management of children with acute gastroenteritis. Curr Opin Gastroen- terol. 2013;29(1):23-30. 
7. Sýkora J, Siala K, Huml M, et al. Evaluation of faecal calpro- tectin as a valuable non-invasive marker in distinguishing gut pathogens in young children with acute gastroenteritis. Acta Paediatr. 2010;99(9):1389-1395. 
8. Duman M, Gencpinar P, Biçmen M, et al. Fecal calprotectin: can be used to distinguish between bacterial and viral gas- troenteritis in children? Am J Emerg Med. 2015;33(10):1436- 1439. 
9. Leung AK, Robson WL. Acute gastroenteritis in children: role of anti-emetic medication for gastroenteritis-related vomiting. Paediatr Drugs. 2007;9(3):175-184. 
10. Freedman SB. Acute infectious pediatric gastroenteritis: beyond oral rehydration therapy. Expert Opin Pharmacother. 2007;8(11):1651-1665. 
11. Levine DA. Antiemetics for acute gastroenteritis in children. Curr Opin Pediatr. 2009;21(3):294-298.
12. Marchetti F, Bonati M, Maestro A, et al. Oral ondansetron versus domperidone for acute gastroenteritis in pediatric emergency departments: multicenter double blind ran- domized controlled trial. PLoS One. 2016;11(11):e0165441. 
13. Freedman SB, Tung C, Cho D, et al. Time-series analysis of ondansetron use in pediatric gastroenteritis. J Pediatr Gastroenterol Nutr. 2012;54(3):381-386. 
14. Magrone T, Jirillo E. The interplay between the gut immune system and microbiota in health and disease: nutraceutical intervention for restoring intestinal homeostasis. Curr Pharm Des. 2013;19(7):1329-1342. 
15. Vandenplas Y, De Greef E, Hauser B, et al. Probiotics and prebiotics in pediatric diarrheal disorders. Expert Opin Phar- macother. 2013;14(4):397-409. 
16. Caffarelli C, Cardinale F, Povesi-Dascola C, et al. Use of pro- biotics in pediatric infectious diseases. Expert Rev Anti Infect Ther. 2015;13(12):1517-1535. 
17. Thomas DW, Greer FR, Committee on Nutrition; Section on Gastroenterology, Hepatology, and Nutrition. Probiotics and prebiotics in pediatrics. Pediatrics. 2010;126(6):1217-1231. 
18. Colletti JE, Brown KM, Sharieff GQ, et al. The management of children with gastroenteritis and dehydration in the emer- gency department. J Emerg Med. 2010;38(5):686-698. 
19. Freedman SB, Willan AR, Boutis K, et al. Effect of dilute apple juice and preferred uids vs electrolyte mainte- nance solution on treatment failure among children with mild gastroenteritis: a randomized clinical trial. JAMA. 2016;315(18):1966-1974. 
20. Granado-Villar D, Cunill-De Sautu B, Granados A. Acute gastroenteritis. Pediatr Rev. 2012;33(11):487-494.
21. Gordon M, Akobeng A. Racecadotril for acute diarrhoea in children: systematic review and meta-analyses. Arch Dis Child. 2016;101(3):234-240. 
22. https://www.nice.org.uk/guidance/cg84/chapter/1-Guidance#antibiotic-therapy

Posted by:

              

     Lakshay Chanana

     

     Speciality Doctor

     Northwick Park Hospital

     Department of Emergency Medicine

     England

     @EMDidactic

  

Postpartum Endometritis

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. 

Posted by:

              

     Lakshay Chanana

     

     Speciality Doctor

     Northwick Park Hospital

     Department of Emergency Medicine

     England

     @EMDidactic

  

Acute Aortic Syndromes

Background

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. 

Risk Factors

• Poorly controlled hypertension
• Connective tissue disorders (eg, Marfan syndrome, Ehlers-Danlos syndrome)
• Congenital valvular disorders (eg, bicuspid aortic valve)
• Aortic coarctation
• Homocystinuria
• Previous cardiac surgery
• Familial aortic dissections, aortic aneurysms
• Pheochromocytoma
• inflammatory vasculitis
• Sympathomimetics (eg, cocaine)
• 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:

1. Friado FJ. Aortic dissection: a 250-year perspective. Tex Heart Inst J. 2011;38(6):694-700. (Review)
2. 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)
3. 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) 
4. Mancini MC. Aortic dissection. Medscape. Available at: http://emedicine.medscape.com/article/2062452-overview.
5. Accessed June 10, 2013. (Review)
6. Hardie AD, Wineman RW, Nandalur KR. The natural his- tory of acute non-traumatic aortic diseases. Emerg Radiol. 2009;16(2):87-95. (Review) 
7. 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) 
8. 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.
9. Lo BM. An evidence-based approach to acute aortic syndromes. Emergency medicine practice. 2013 Dec 1;15(12):1-23.

Posted by:

              

     Lakshay Chanana

     

     Speciality Doctor

     Northwick Park Hospital

     Department of Emergency Medicine

     England

     @EMDidactic

  

The "qRBBB" pattern

Presence of qRBBB in the setting of acute coronary syndrome signifies proximal 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
• Delayed intrinsicoid deflection time 

RBBB (Image from LIFTL)

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:

1. 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. 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.
3. 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.
4. 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. 
5. http://hqmeded-ecg.blogspot.co.uk/2010/01/right-bundle-branch-block-with-subtle.html
6. http://hqmeded-ecg.blogspot.co.uk/2017/04/rbbb-with-transient-st-elevation.html
7. http://hqmeded-ecg.blogspot.co.uk/2010/11/wide-complex-tachycardia-its-really.html
8. http://hqmeded-ecg.blogspot.co.uk/2014/03/elderly-woman-in-shock-ekg-from.html
9. https://emcrit.org/wp-content/uploads/2015/03/Who-to-PCI-by-Smith-and-Weingart.pdf
10. https://lifeinthefastlane.com/ecg-library/basics/right-bundle-branch-block/

Posted by:

              

     Lakshay Chanana

     

     Speciality Doctor

     Northwick Park Hospital

     Department of Emergency Medicine

     England

     @EMDidactic