Category: Neurological Emergencies

Question Of The Day #44

question of the day
~ Joseph Ciano, USA ~ Leave a comment

Which of the following is the most appropriate next investigation to confirm this patient’s diagnosis?

  • A) Lumbar puncture
  • B) 12-lead EKG
  • C) MRI of brain
  • D) Noncontrast CT scan of head

This patient presents to the Emergency Department with altered mental status.  This presenting symptom can be due to a large variety of etiologies, including hypoglycemia, sepsis, toxic ingestions, electrolyte abnormalities, stroke, and more.  The management and evaluation of a patient with altered mental status depends on the primary assessment of the patient (“ABCs”, or Airway, Breathing, Circulation) to identify any acute life-threatening conditions that need to be managed emergently, the history, and the physical examination.  One mnemonic that may help in remembering the many causes of altered mental status is “AEIOUTIPS”.  The table below outlines this mnemonic.

ALTERED MENTAL STATUS

The information provided indicates that the patient’s headache was maximal at onset, severe, associated with vomiting, and led to a deteriorating mental status ultimately requiring intubation.  This history is very concerning for intracranial bleeding, especially subarachnoid hemorrhage (SAH).  The majority of atraumatic SAHs are caused by the rupture of a saccular aneurysm.  This causes the leakage of blood into the subarachnoid space.  Symptoms of a SAH are sudden onset headache that is maximal intensity at onset (“thunderclap headache”), syncope, vomiting, seizures, and any neurological deficits.  Risk factors for SAH are age over 50years-old, family history of SAH, alcohol abuse, tobacco smoking, Marfan Syndrome, Ehlers-Danlos Syndrome, and Polycystic Kidney Disease.  Diagnosis of SAH takes into account the patient’s history, physical exam, and risk factors. 

Patients that arrive in the Emergency Department under 6hours since symptom onset should initially get a noncontrast CT scan of the head (Choice D).  When a noncontrast head CT is performed in this time window, its sensitivity reaches 98-100%.  Noncontrast head CTs performed within the first 24hrs since headache onset have a sensitivity of about 90%.  Patients with signs and symptoms concerning for SAH who have a negative CT head should get a lumbar puncture (Choice A) to evaluate for xanthochromia.  This is especially important if the patient’s symptoms have been for over 6 hours.  A 12-lead EKG (Choice B) can show ST and T wave changes, but an EKG alone cannot be used to make a diagnosis of SAH.  A brain MRI (Choice C) can make the diagnosis of SAH, but a CT scan would be preferred due to greater CT scan accessibility, cost, and the shorter time of this imaging test.  The best next investigation would be a noncontrast CT of the head (Choice D).

Correct Answer: D

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References

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Question Of The Day #43

question of the day
~ Joseph Ciano, USA ~ Leave a comment

Which of the following is the most likely cause for this patient’s altered mental status?

  • A) Diabetic ketoacidosis
  • B) Sepsis
  • C) Intracerebral hemorrhage
  • D) Hypothyroidism

This patient presents to the Emergency Department with altered mental status and fever.  Altered mental status can be due to a large variety of etiologies, including hypoglycemia, sepsis, toxic ingestions, electrolyte abnormalities, stroke, and more.  The management and evaluation of a patient with altered mental status depends on the primary assessment of the patient (“ABCs”, or Airway, Breathing, Circulation) to identify any acute life-threatening conditions that need to be managed emergently, the history, and the physical examination.  One mnemonic that may help in remembering the many causes of altered mental status is “AEIOUTIPS”.  The table below outlines this mnemonic.

ALTERED MENTAL STATUS

This patient has confusion, fever, lower abdominal pain, dysuria, and no focal neurological deficits on exam.  Diabetic ketoacidosis (Choice A) is unlikely as the patient does not have marked hyperglycemia (>250mg/dL (13.8mmol/L)), polyuria, or polydipsia.  Intracranial hemorrhage (Choice C) is unlikely as the patient has no headache, history of trauma, focal neurologic deficits, or coma.  Severe hypothyroidism (Choice D), known as myxedema coma, can cause altered mental status.  This condition is marked by somnolence or coma, hypothermia, nonpitting edema on the hands and feet, dry skin, macroglossia (enlarged tongue), and hair loss.  This patient does not have symptoms consistent with severe hypothyroidism. 

Sepsis (Choice B), especially in elderly individuals, can cause altered mental status.  The patient’s fever, confusion, lower abdominal pain, and dysuria all point to a likely diagnosis of urosepsis.  Sepsis is the most likely cause of this patient’s disoriented state.  Treatment with early IV hydration and antibiotics will help remedy the patient’s altered mental status.  Correct Answer: B

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References

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Question Of The Day #42

question of the day
~ Joseph Ciano, USA ~ Leave a comment

Which of the following is the most appropriate next step in management for this patient’s condition?

  • A) IV insulin continuous infusion
  • B) IV hypertonic 3% NaCl
  • C) IV 0.9% NaCl bolus
  • D) IV insulin bolus

This patient presents to the Emergency Department with altered mental status.  This presenting symptom can be due to a large variety of etiologies, including hypoglycemia, sepsis, toxic ingestions, electrolyte abnormalities, stroke, and more.  The management and evaluation of a patient with altered mental status depends on the primary assessment of the patient (“ABCs”, or Airway, Breathing, Circulation) to identify any acute life-threatening conditions that need to be managed emergently, the history, and the physical examination.  One mnemonic that may help in remembering the many causes of altered mental status is “AEIOUTIPS”.  The table below outlines this mnemonic.

ALTERED MENTAL STATUS

This patient has a markedly elevated glucose level.  All patients with altered mental status should have a point of care glucose test as both hypoglycemia and severe hyperglycemia can cause altered mental status.  Some diagnoses to consider in this patient are diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS).  Both of these diagnoses can present with hyperglycemia and altered mental status, but HHS more often presents with higher glucose levels (greater than 600mg/dL (33mmol/L)) and more pronounced Central Nervous System depression.  Patients with HHS may have severe somnolence to the point of coma and may require intubation for airway protection.  In both DKA and HHS, patients are severely dehydrated by osmotic diuresis.  High glucose levels in the serum create an osmotic gradient that causes increased urination and fluid loss.  The first step in treatment for DKA and HHS is volume resuscitation. 

IV fluids (Choice C) should be given prior to the initiation of insulin therapy (Choices A and D).  After adequate IV hydration and correction of electrolyte derangements, insulin can be started to normalize glucose levels.  Bolus doses of IV insulin (Choice D) are harmful in both DKA and HHS and increase the risk of cerebral edema development.  For this reason, an IV insulin continuous infusion (Choice A) is always preferred over an insulin bolus (Choice D).  IV hypertonic 3% NaCl (Choice B) is the treatment for severe hyponatremia causing altered mental status or seizure.  Severe hyperglycemia can cause pseudohyponatremia, but this can be corrected for using the standard sodium correction formula (see references below).  The question stem provides an explanation for this patient’s altered mental status (hyperglycemia), so hypertonic saline should not be given with the information provided.  IV fluid administration (Choice C) is the next best step. Correct Answer: C

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References

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Question Of The Day #41

question of the day
~ Joseph Ciano, USA ~ Leave a comment

Which of the following is the most appropriate next step in management for this patient?

  • A) CT scan of head without contrast
  • B) IV hypertonic 3% NaCl
  • C) IV dextrose
  • D) IV potassium chloride

This patient presents to the Emergency Department with altered mental status. This presenting symptom can be due to a large variety of etiologies, including hypoglycemia, sepsis, toxic ingestions, electrolyte abnormalities, stroke, and more. The management and evaluation of a patient with altered mental status depend on the primary assessment of the patient (“ABCs,” or Airway, Breathing, Circulation) to identify any acute life-threatening conditions that need to be managed emergently, the history, and the physical examination. One mnemonic that may help in remembering the many causes of altered mental status is “AEIOUTIPS.” The infographic below outlines this mnemonic.

ALTERED MENTAL STATUS

This patient is awake and moving all extremities, but with obvious confusion and dysarthria. Ordering a CT scan of the head without contrast (Choice A) may be helpful in this patient to evaluate for intracerebral hemorrhage, stroke, or a brain mass. However, the question stem indicates that this patient has a low glucose level. Glucose is considered low at levels below 70mg/dL (3.9 mmol/L); however, the absence of any symptoms can be reassuring. Glucose levels that are more severely low (less than 40mg/dL (2.2 mmol/L)) are more concerning than levels that are only moderately low (less than 70mg/dL (3.9mmol/L)). All patients with altered mental status should have a point of care glucose test. Both hypoglycemia and severe hyperglycemia can cause altered mental status. Hypoglycemia, if left untreated, can cause permanent brain damage. For this reason, the prompt identification of low blood glucose is critical so it can be treated rapidly.

Administration of IV hypertonic 3% NaCl (Choice B) would be helpful in a patient with severe hyponatremia with altered mental status or seizure. However, the question stem provides a cause for the patient’s symptoms (low glucose). IV potassium chloride (Choice D) would be helpful in the case of hyperkalemia to stabilize the cardiac membrane. Severe hyperkalemia can cause weakness and arrythmias, but does not cause dysarthria. This patient is at higher risk for hyperkalemia as he is a hemodialysis patient, but no evidence is given that he has hyperkalemia (i.e., peaked T waves on EKG or widened QRS interval). Again, a low glucose level is given in the question stem, which should be treated first.

IV dextrose (Choice C) is the best next step in management for this patient’s hypoglycemia. This patient has had poor oral intake and has end-stage renal disease. Insulin is excreted by the kidneys, so patients with end-stage renal disease are more prone to insulin “buildup” and hypoglycemia. In addition to administering IV dextrose (i.e., D50 bolus), providing food with complex carbohydrates is important to prevent recurring hypoglycemic episodes. If the patient continues to have persistent hypoglycemia despite an IV dextrose bolus and food, a continuous IV dextrose infusion (i.e., D10W at 100cc/hour) and admission for further evaluation should be considered. Correct Answer: C

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References

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Special Populations in the ED: Athletes

special populations in the ED athletes
~ Arthur Martins, Brasil ~ Leave a comment

It is common to hear that “when you work in an Emergency Department (ED), you have to be prepared for everything”. In my experience as a medical student, this could not be more true. I’ve seen tea overdose, collision scooter vs horse, and anything in between. All these experiences will contribute to my formation and made me realize that we are not prepared for many situations. Some of these situations may involve specific populations we’re not so familiarized with and sometimes can change the way we manage an emergency.

Here, I want to discuss some of these “special populations” which may demand a different approach than the usual – and that is what makes emergency medicine so interesting. Let’s talk about one of these subgroups of patients: athletes, and what makes them unique.

Athletes: What do I need to know about them?

  • Heart and Hemodynamic: The “athlete’s heart syndrome (1)”
    • Morphological, functional and electrical changes
      • Lower heart rate;
      • Hypertrophic left ventricle (LV)
      • Lifelong cardiac remodelling could lead to arrhythmogenic pathways
  • Changes in autonomic nervous system – vagal tonus
  • Pulmonary efficiency:
    • Unlike what may be the first thought, the respiratory system does not differ greatly in athletes from non-athletes (2).
  • High energy trauma:
    • Be aware that professional athletes are constantly at risk of high energy traumas, in special head traumas (concussions) and limb trauma (fractures);

How could this be a problem?

  • Late signs of hypovolemia
    • The athlete’s autonomic nervous system has pronounced vagal tonus, which leads to the famous resting bradycardia – this could disguise a tachycardia, one of the early signs of hypovolemia (2).
  • Delay in seeking help
    • Elite athletes may delay seeking help or admit they are not feeling well for fear of losing a competition or training sessions.
    • Besides that, in amateur (and sometimes even in professional) level competitions, staff and coaches often are not trained to identify conditions that need prompt medical assistance

Common situations and how to manage

Exercise and health always have been put together in a “cause and consequence” relation. Besides their undeniable positive effects, exercise on the professional level also has its sidebacks and associated risks. Here I want to discuss some physiological changes we observe in the elite athletes and a very common condition in the ED: the sport-related concussion.

Sport-related concussion (3,4) is a traumatic brain injury induced by biomechanical forces. It may be caused either by a direct impact to the head or by a force transmitted from the impact elsewhere in the body; It typically presents with rapid onset of short-lived signs and symptoms; However, the course is sometimes unpredictable and may evolve in minutes to hours; It may or may not have a decreased level of counsciousnes.

The current literature organize the signs and symptoms of sport-related concussion in 4 domains

  1. Somatic
    • Headache, dizziness, gait disturbances, vertigo, nausea and vomiting, near vision impairment
  2. Cognitive
    • Impaired memory (amnesia), slowed speech, confusion,
  3. Sleep
    • Insomnia
  4. Emotional
    • Irritability, labile humour

Given the rapid onset and short duration, the patient might present to the ED with minor or no symptoms; However, the emergency physician still plays an important role, providing supportive care to relieve remaining symptoms and rule out more severe conditions.

Attention

  • Due to the mechanism of trauma, always rule out cervical spine lesions or instability.
  • Also, signs of basilar skull fracture (racoon eyes, Battle’s sign, CSF rhinorrhea)
  • A Glasgow Coma Scale < 13 should raise awareness for a more severe brain lesion.
  • Does this patient need a head CT?
    • Canadian CT head rule (adults)
    • PECARN CT rule (under 16)   

Management (4)

Headache: 86% had significant pain reduction, and 52% had complete headache resolution after receiving an intravenous dose of one or more of the following: ketorolac, prochlorperazine, metoclopramide, chlorpromazine, and ondansetron. Common orally administered analgesics such acetaminophen, non-steroidal anti-inflammatories and triptans have shown efficacy for pain relief, but there are no studies in the ED setting.
 
Dizziness: Suspicion for peripheral vertigo can be confirmed by the Dix-Hallpike manoeuvre and treated with the Epley manoeuvre. Meclizine (vestibular suppressant) and diazepam can be used with caution because of potential side effects on cognition and alertness.
 
To date, rest continues to be recommended for the acute (24-48h) injury period. After that period, patients can be encouraged to become gradually more active, always below their cognitive and physical limits.

When to admit

This decision is based on the patient’s clinical status. Persistent symptoms and alterations on head CT are the most common indications for admission. 
 
Discharging to home: Education is key for recovery and prevention of recurrence (4). Current evidence indicates that written educational material is more effective than orally given instructions only; Important information that should be present in the educational material are expected symptoms, their management and a timeframe of resolution. 
[cite]

Recent Blog Posts by Arthur Martins

References and Further Reading

  1. Carbone A, D’Andrea A, Riegler L, Scarafile R, Pezzullo E, Martone F, America R, Liccardo B, Galderisi M, Bossone E, Calabrò R. Cardiac damage in athlete’s heart: When the “supernormal” heart fails! World J Cardiol 2017; 9(6): 470-480 Available from: URL: http://www.wjgnet.com/1949-8462/full/v9/i6/470.htm DOI: http://
    dx.doi.org/10.4330/wjc.v9.i6.470
  2. ACSM’s advanced exercise physiology. — 2nd ed.;Peter A. Farrell, Michael Joyner, Vincent Caiozzo ISBN 978-0-7817-9780-1
  3. McCrory P, Meeuwisse W, Dvorak J, et al. Br J Sports Med 2018;51:838–847
  4. Bazarian JJ, Raukar N, Devera G, et al. Recommendations for the Emergency Department Prevention of Sport-Related Concussion. Ann Emerg Med. 2020;75(4):471-482. doi:10.1016/j.annemergmed.2019.05.032

Saturday Night Palsy: A Case Discussion

Saturday Night Palsy
~ Maryam Bagherzadeh, Canada ~ Leave a comment

Case Presentation

In his mid-twenties, a patient presents to the emergency department with a profound drop in their wrist and some paresthesia to the dorsal of his hand. He is otherwise fit and healthy. When taking the history, he gives the classic story of having a few too many drinks the night before and falling sleep on a chair in an uncomfortable position, with his arm draped over the edge of the chair. When he woke up the next day, he felt a dull pain in their upper arm and could not extend his wrist. The patient attempted to neglect the problem and tried to do some exercises to alleviate the pain. However, two hours later, his arm remained quite flaccid to extension. The patient began to worry and presented to the emergency department.

saturday-night-palsy
https://nabilebraheim.wordpress.com/2018/02/14/radial-nerve-injury-locations/

Saturday Night Palsy

Saturday night palsy refers to a compressive neuropathy of the radial nerve that occurs due to prolonged and direct pressure to the upper medial arm by an object or a surface [1]. The radial nerve originates from the brachial plexus, carrying fibres from the C5-T1 ventral nerve roots. It innervates the medial and lateral heads of the triceps brachii muscle, as well as all twelve muscles in the posterior osteofascial compartments of the forearm. It provides motor innervation to the dorsal arm muscles and extrinsic extensors of the wrist and hand, as well as sensory innervation to most of the back of the hand (except the back of the 5th digit and adjacent half of 4th digit) [2].

saturday night palsy - wrist drop
http://ksumsc.com/download_center/Archive/1st/438/2.%20Musculoskeletal%20Block/Male/Anatomy/Radial%20%26%20Ulnar%202018-.pdf

Saturday night palsy is also known as the “honeymoon palsy”, which describes an event where an individual falls to sleep on their partner’s arm, compressing the person’s radial nerve for an extended period. Other terms for Saturday night palsy include “lover’s palsy”,” park bench palsy” and “crutch palsy”. Essentially, Saturday night palsy can be caused by any unnatural positioning or use of equipment that compresses the radial nerve, which is where the terms have originated from [1,3].

History and Physical Examination

As described in the case above, patients often report symptoms following excessive alcohol consumption and sleeping in an unnatural position. Otherwise, they may report other mechanisms in which their inner arm may have been compressed. Sometimes, symptoms do not present until several days after the nerve compression, making the diagnosis of this presentation difficult. Patients can also report other symptoms such as weakness, numbness, tingling and pain in the arm [1].

On physical exam, patients present with a characteristic wrist drop and inability to extend the wrist and fingers to the metacarpophalangeal joints’ level. Patients may also present with loss of triceps reflex, and sensory deficits involving the back of the hand [1,4].

Investigations

Saturday night palsy is mainly a clinical diagnosis and does not require further investigative measures. However, some tools may help evaluate differential diagnoses and prognosis of the presenting condition. Electromyography and nerve conduction studies may localize the lesion and help differentiate between other neuropathies such as the brachial plexus or peripheral neuropathies. Ultrasound is a low-cost and low-risk method that can help visualize the nerve and identify areas of damage. MRI can assist in visualizing the finer details that may not be noticeable on ultrasound, as well as other presenting problems such as soft-tissue masses. The X-ray can guide in assessing for fractures and dislocations that may be causing the nerve compressions [1,5]. While none of these measures is necessary for diagnosing Saturday night palsy, it may be worthwhile to consider them for individual patients that require further investigations and where other diagnoses are being considered.

Management

Treatment of Saturday night palsy is mainly through physical therapy, involving a dynamic splint that holds the arm in extension and allows for full passive range of motion during use. This can be complemented with the help of supportive care, including analgesics such as non-steroidal anti-inflammatory drugs (NSAIDs), resting the arm, corticosteroids use, and steroid injections [2]. To prevent re-injury of the nerve, it is important to counsel the patient on not repeating the same mechanism that caused the initial neural compression. Patients should also be counseled on the importance of physical therapy and following up in case of delayed recovery, which may necessitate other considerations such as surgical interventions [1,2].

References and Further Reading

  1. Ansari FH, Juergens AL. Saturday Night Palsy. [Updated 2020 May 13]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK557520/
  2. Bumbasirevic, M., Palibrk, T., Lesic, A., & Atkinson, H. D. (2016). Radial nerve palsy. EFORT open reviews, 1(8), 286-294.
  3. Latef, T. J., Bilal, M., Vetter, M., Iwanaga, J., Oskouian, R. J., & Tubbs, R. S. (2018). Injury of the radial nerve in the arm: A review. Cureus, 10(2).
  4. DeCastro A, Keefe P. Wrist Drop. [Updated 2020 Jul 21]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK532993/
  5. Agarwal, A., Chandra, A., Jaipal, U., & Saini, N. (2018). A panorama of radial nerve pathologies-an imaging diagnosis: a step ahead. Insights into imaging, 9(6), 1021-1034.
[cite]

Recent Blog Posts by Maryam Bagherzadeh

Question Of The Day #26

question of the day
~ Joseph Ciano, USA ~ Leave a comment
qod26
38 - atrial fibrillation

Which of the following is the most appropriate next step in management for this patient’s condition?

  • A) Electrical cardioversion
  • B) Intravenous metoprolol
  • C) General observation
  • D) Intravenous adenosine

This patient presents to the emergency department with palpitations, a narrow complex tachycardia (<120msec), and an irregularly irregular rhythm. A close look at this patient’s EKG reveals the absence of discrete P waves and QRS complexes that are spaced at varying distances from each other (most apparent in lead V6). These signs support a diagnosis of Atrial Fibrillation, or “AFib.” Atrial Fibrillation is an arrhythmia characterized by an irregularly irregular rhythm, the absence of P waves with a flat or undulating baseline, and narrow QRS complexes. Wide-QRS complexes may be present in AFib if there is a concurrent bundle branch block or Wolff-Parkinson White Syndrome. AFib is caused by the electric firing of multiple ectopic foci in the atria of the heart. This condition is triggered by a multitude of causes, including ischemic heart disease, valvular heart disease, dilated or hypertrophic cardiomyopathies (likely related to this patient’s congestive heart failure history), sepsis, hyperthyroidism, excess caffeine or alcohol intake, pulmonary embolism, and electrolyte abnormalities.

The main risk in AFib is the creation of thrombi in the atria as they fibrillate, resulting in emboli that travel to the brain and cause a stroke. The CHA2DS2VASc scoring system is used to risk stratify patients and determine if they require anticoagulation to prevent against thrombo-embolic phenomenon (i.e. stroke). This patient has a high CHA2DS2VASc score, so she would require anticoagulation. In addition to anticoagulation, A fib is treated with rate control (i.e. beta blockers or calcium channel blockers), rhythm control (i.e. anti-arrhythmic agents), or electrical cardioversion. Electrical cardioversion (choice A) is typically avoided when symptoms occur greater than 48 hours, since the risk of thrombo-emboli formation is higher in this scenario. An exception to this would be a patient with “unstable” AFib. Signs of instability in any tachyarrhythmia are hypotension, altered mental status, or ischemic chest pain. This patient lacks all of these signs and symptoms. Although this patient lacks signs of instability, this patient’s marked tachycardia should be addressed with medical treatment. General observation (Choice C) is not the best choice for this reason. Intravenous adenosine (Choice D) is the best choice for a patient with supraventricular tachycardia (SVT). This is a narrow-complex AV nodal re-entry tachycardia with rates that range from 120-280bpm. SVT also lacks discrete P waves. A key factor that differentiates A fib from SVT is that SVT has a regular rhythm, while AFib has an irregular rhythm. Intravenous metoprolol (Choice B) is the best treatment option listed in order to decrease the patient’s heart rate.

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References

  • Brady W.J., & Glass III G.F. (2020). Cardiac rhythm disturbances. Tintinalli J.E., Ma O, Yealy D.M., Meckler G.D., Stapczynski J, Cline D.M., & Thomas S.H.(Eds.), Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9e. McGraw-Hill. https://accessmedicine.mhmedical.com/content.aspx?bookid=2353&sectionid=218687685
  • Burns, E. (2020) Atrial Fibrillation. Life in The Fast Lane. Retrieved from https://litfl.com/atrial-fibrillation-ecg-library/

 

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iEM Image Feed: Camel Bite

iem image feed camel bite
~ iEM Education Project Team ~ Leave a comment
camel bite injury

EMS brought a 24-year-old man due to camel bite happened while feeding the camel in the early morning. The injury was basically on the right arm and forearm. No other injuries, vitally stable.

Students should know the following while taking care of these patients.

  1. Systematic evaluation of the patient – remember ATLS, primary and secondary survey.
  2. Focused neurologic and vascular examination.
  3. Exposing the wound and ordering an x-ray
  4. Wound cleaning and management
  5. Be aware of fracture – Open Fracture!
  6. Antibiotic coverage and tetanus toxoid/IG
  7. For open fractures – Look for Gustilo-Anderson Classification and choose appropriate antibiotics.  
  8. Do not forget – pain medication.
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Question Of The Day #25

question of the day
~ Joseph Ciano, USA ~ Leave a comment
qod25
835 - 3rd degree heart block

Which of the following is the most likely diagnosis of this patient’s condition?

  • A) Sinus bradycardia
  • B) First-Degree AV Block
  • C) Second-Degree AV Block (Mobitz type II)
  • D) Third-Degree AV Block

This patient has marked bradycardia on exam with a borderline low blood pressure. These vital sign abnormalities are likely the cause of the patient’s dizziness. Bradycardia is defined as any heart rate under 60 beats/min. The most common cause of bradycardia is sinus bradycardia (Choice A). Other types of bradycardia include conduction blocks (i.e. type 2 or type 3 AV blocks), junctional rhythms (lack of P waves with slow SA nodal conduction), idioventricular rhythms (wide QRS complex rhythms that originate from the ventricles, not atria), or low atrial fibrillation or atrial flutter. About 80% of all bradycardias are caused by factors external to the cardiac conduction system, such as hypoxia, drug effects (i.e., beta block or calcium channel blocker use or overdose), or acute coronary syndromes.

ecg qod25Sinus bradycardia (Choice A) occurs when the electrical impulse originates from the SA node in the atria. Signs of sinus bradycardia on EKG are the presence of a P wave prior to every QRS complex. This EKG shows P waves prior to each QRS complex, but there are extra P waves that are not followed by QRS complexes. Some P waves are “buried” within QRS complexes or within T waves. The EKG below marks each P wave with a red line and each QRS complex with a blue line.

 

First-degree AV Block (Choice B) is a benign arrhythmia characterized by a prolonged PR interval. This patient’s EKG has variable PR intervals (some prolonged, some normal). This is a result of a more severe AV conduction block. Second-Degree AV Blocks are divided into Mobitz type I and Mobitz Type II. Mobitz type I, also known as Wenckebach, is characterized by a progressive lengthening PR interval followed by a dropped QRS complex. This can be remembered by the phrase, “longer, longer, longer, drop.” Wenckebach is a benign arrhythmia that does not typically require any treatment. Mobitz type II (Choice C) is characterized by a normal PR interval with random intermittent dropping of QRS complexes. This patient’s EKG has consistent spacing between each QRS complex (blue lines) and consistent spacing between each P wave (red lines). However, the P waves and QRS complexes are not associated with each other. This phenomenon is known as AV dissociation. These EKG changes are signs of a complete heart block, also known as Third-Degree AV Block (Choice D). Both Second-Degree AV block- Mobitz type II (Choice C) and Third-Degree AV Block (Choice D) are more serious conduction blocks that require cardiac pacemakers. Correct Answer: D

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References

  • Brady W.J., & Glass III G.F. (2020). Cardiac rhythm disturbances. Tintinalli J.E., Ma O, Yealy D.M., Meckler G.D., Stapczynski J, Cline D.M., & Thomas S.H.(Eds.), Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9e. McGraw-Hill. https://accessmedicine.mhmedical.com/content.aspx?bookid=2353&sectionid=218687685
  • Nickson, C. (2020). Heart Block and Conduction Abnormalities. Life in the Fast Lane. Retrieved from https://litfl.com/heart-block-and-conduction-abnormalities/

 

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Pathological Brain CT Findings – Illustration

Pathological Brain CT Findings
~ Murat Yazici, Turkey ~ Leave a comment

In this post, we will share the traumatic (Epidural, subdural, cerebral contusion, subarachnoid hemorrhage, cerebral edema) and atraumatic (intracranial parenchymal hemorrhage, subarachnoid hemorrhage) brain computerized tomography (CT) findings. We will also provide GIF images and one final image, which includes all pathologies in one image.

ATRAUMATIC PATHOLOGICAL BRAIN CT FINDINGS

TRAUMATIC PATHOLOGICAL BRAIN CT FINDINGS

ATRAUMATIC PATHOLOGICAL BRAIN CT FINDINGS – GIF

TRAUMATIC PATHOLOGICAL BRAIN CT FINDINGS  – GIF

PATHOLOGICAL BRAIN CT FINDINGS  – ONE POST

References and Further Reading

  1. https://iem-student.org/2019/09/04/cranial-ct-anatomy-a-simple-image-guide-for-medical-students/
  2. The Atlas of Emergency Radiology
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Hypokalemic Periodic Paralysis in the ED

Hypokalemic Periodic Paralysis in the ED
~ Sumaiya Hafiz, UAE ~ 1 Comment

Case Presentation

A middle-aged man with a two days history of weakness in his legs. The patient works as a construction worker and is used to conducting heavy physical activity.

After a thorough history and examination, the weakness was reported in the lower extremities with a power of 2/5, whereas the power in upper extremities was 4.5/5, Achilles tendon reflex was reduced, plantar response and other reflexes were intact, with normal sensation. Rest of the examination is unremarkable.

The vitals are within normal ranges, Blood investigations include – Urea and electrolytes, liver and renal function, full blood count, thyroid function tests, creatine kinase, urine myoglobin, vitamin B12 and folic acid levels.

Potassium level was 1.7 mEq/L (normal 3.5-5.5), and all other parameters were within normal ranges.

The ECG showed inverted T waves and the presence of U waves. An Example of an ECG:

ECG-hypokalemia

Hypokalaemia

Hypokalemic periodic paralysis is a rare disorder that may be hereditary as the primary cause, or secondary due to thyroid disease, strenuous physical activity, a carbohydrate-rich meal and toxins. The patients are mostly of Asian origin.

The most common presentation is of symmetrical weakness in lower limbs, with a low potassium level and ECG changes of hypokalemia. The patients may have a history of similar weaknesses which may be several years old. An attack may be triggered by infections, stress, exercise and other stress-related factors.

The word ‘weakness’, can lead to physicians thinking about stroke, neurological deficits and other life-threatening illnesses such as spinal cord injuries associated with high morbidity and mortality which need to be ruled out in the ED.

In this case, history and examination are vital. Weakness in other parts of the body, a thorough neurological examination are important aspects.

Patients are monitored and treated with potassium supplements (oral/Intravenous) until the levels normalize. ECG monitoring is essential, as cardiac function may be affected. 

The patient should be examined to assess the strength and should be referred for further evaluation and to confirm the diagnosis.

The differential diagnosis for weakness in lower limb include :

  1. Spinal cord disease (https://iem-student.org/spine-injuries/)
  2. Guillain barre syndrome
  3. Toxic myositis
  4. Trauma
  5. Neuropathy
  6. Spinal cord tumour

References

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Doctor, My Head Hurts!

DOCTOR, MY HEAD HURTS
~ Arthur Martins, Brasil ~ Leave a comment

February was the last of my three months at Family Medicine clinical rotation. In addition to normal clinical consultations, we also had to take turns attending spontaneous demands coming “from the street”, in a primary care resource center that works similar to a green zone setting in the ED. During these three months, I’ve noticed that, sometimes, the easiest patient to manage is that one with a major complaint like chest pain, severe dyspnea, altered mental status, and so on. Things become more difficult, however, when you have a patient that has just a headache, a very common symptom, but one that could be related to an enormous variety of conditions, some of which life-threatening. Sometimes, you dig under the “green” patient and discover a secret “yellow” or even a “red” condition.

Next, I will try to put some light on the investigation of one of the most common complaints I’ve seen, and one of the symptoms that always put a bug in the ear: Headache.

Epidemiology

Headache is a very common complaint at the Emergency Department, being the fifth leading cause of ED visits¹. Alarmingly, about 0.5% of patients who had presented with a headache and discharged home have returned with a serious condition, of which 18% were acute ischemic stroke.²

Clinical Presentation

Patients can describe headache, a very nonspecific and hard to clarify complaint, in diverse ways, ranging from saying solely “my head hurts” to making a circular gesture around his/her head with. Therefore, identifying potential risk factors that can alert us to potential adverse outcomes. Here are a few decision rules for patients with headache:

SNNOOP10

The mnemonic SNNOOP10³ refers to the red flag symptom and findings to screen, which may point to related secondary headaches.

snnoop10

Ottawa Subarachnoid Hemorrhage Rule

Ottawa Subarachnoid Hemorrhage Rule fundamentally helps to rule out (Sensitivity: 100% Specificity: 15%) subarachnoid hemorrhage (SAH) in patients with headache. You can apply this rule ONLY IF:

  • The patient is alert and older than 15 years old with
  • New severe non-traumatic headache, reaching maximum intensity within 1 hour and
  • NO new neurological deficits, no history of intracranial tumors, previous SAH or aneurysms, and similar headaches (≥ 3 episodes over ≥ 6 months)

Risk factors are:

  1. Age ≥ 40
  2. Neck pain or stiffness
  3. Witnessed loss of consciousness
  4. Onset during exertion
  5. “Thunderclap headache” (defined as instantly and immediately peaked pain)
  6. Limited neck flexion on examination (defined as the inability to touch chin to chest or raise head 3 cm off the bed if supine)

If ANY of these factors is present, SAH can not be ruled out, and this patient needs further investigation. A recent study has assessed the performance of the Ottawa decision rule for patients presenting with headache in the ED, showing that it is a highly sensitive test (100%), making it useful in order to “not miss the disguised red patient.”5 Not by coincidence, Tintinalli’s book states with bold letters: “Acute onset of a severe headache is subarachnoid hemorrhage until proven otherwise.”

Acute onset of a severe headache is subarachnoid hemorrhage until proven otherwise.

Tintinalli's Comprehensive Study Guide Tweet

Investigation

Neuroimaging is a valuable diagnostic tool but is also an expensive one. Besides, it can be harmful due to radiation exposure or contrast use.

There is a lot of controversy in the literature regarding the question “When to image patients with a headache?”, but the consensus is to image when a patient presents with red flags, especially those related to vascular causes, raised intracranial pressure and focal signs.4

CT scan is the preferred method to investigate SAH, with excellent sensitivity and specificity (both bigger than 90%) in the first 6 hours of hemorrhage.6 However, if more time has passed, other diagnostic tools will probably be required in this case. Also, as said before, the costs are a major factor regarding neuroimaging, and sometimes you have to use what you have.

Lumbar Puncture

  • Indications7:
    • Suspected infectious disease of the CNS
    • Suspected SAH
    • Suspected idiopathic intracranial hypertension – as diagnostic and treatment
  • Contraindications7:
    • Coagulopathy (including anticoagulant drugs) or thrombocytopenia
    • Infection at the puncture site
    • Suspected epidural abscess
    • Findings on the CT scan to deferring LP
    • Brainstem herniation
    • Mass with signs of compression of the 4th ventricle
    • Signs of increased intracranial pressure or midline shift
    • Acute intracranial hematoma

Disposition and Follow-up(7,8)

  • Most patients can be discharged with a simple painkiller prescription. About 95% of patients presenting to the ED with headache have a benign etiology and don’t need further investigation in the ED.
  • The acute benign headache usually resolves with acetaminophen, NSAIDs, hydration, and rest.
  • An adequate follow-up plan is a good practice since most headaches are due to chronic conditions that may benefit from pharmacologic prophylaxis as well as lifestyle modifications.

This subject is open to discussion. Although it looks (and it is) a simple and easy-to-manage condition 90% of times, it has the potential to give the doctor some headache, too!

References and Further Reading

  1. American College of Emergency Physicians Clinical Policies Subcommittee (Writing Committee) on Acute Headache:, Godwin, S. A., Cherkas, D. S., Panagos, P. D., Shih, R. D., Byyny, R., & Wolf, S. J. (2019). Clinical Policy: Critical Issues in the Evaluation and Management of Adult Patients Presenting to the Emergency Department With Acute Headache. Annals of emergency medicine, 74(4), e41–e74. https://doi.org/10.1016/j.annemergmed.2019.07.009
  2. Dubosh, N. M., Edlow, J. A., Goto, T., Camargo, C. A., Jr, & Hasegawa, K. (2019). Missed Serious Neurologic Conditions in Emergency Department Patients Discharged With Nonspecific Diagnoses of Headache or Back Pain. Annals of emergency medicine, 74(4), 549–561. https://doi.org/10.1016/j.annemergmed.2019.01.020
  3. Do, T. P., Remmers, A., Schytz, H. W., Schankin, C., Nelson, S. E., Obermann, M., Hansen, J. M., Sinclair, A. J., Gantenbein, A. R., & Schoonman, G. G. (2019). Red and orange flags for secondary headaches in clinical practice: SNNOOP10 list. Neurology, 92(3), 134–144. https://doi.org/10.1212/WNL.0000000000006697
  4. Good C. (2019). British Society Of Neuroradiologists Guidelines for Headache. Retrieved July 23, 2020, from https://bsnr.org.uk/_userfiles/pages/files/standards_and_guidelines/bsnr_guidelines_for_imaging_in_headache_april_2019_final.pdf
  5. Wu, W. T., Pan, H. Y., Wu, K. H., Huang, Y. S., Wu, C. H., & Cheng, F. J. (2020). The Ottawa subarachnoid hemorrhage clinical decision rule for classifying emergency department headache patients. The American journal of emergency medicine, 38(2), 198–202. https://doi.org/10.1016/j.ajem.2019.02.003
  6. Kwiatkowski T. and Friedman B. W. (2018). Headache Disorders. In: R. M. Walls, R. S. Hockberger, M. Gausche-Hill, K. Bakes, J. M. Baren, T. B. Erickson, A. S. Jagoda, A. H. Kaji, M. VanRooyen, R. D. Zane, (Eds.) Rosen’s Emergency Medicine Concepts and Clinical Practice (9th ed. pp: 1265-1277). Philadelphia, PA: Elsevier.
  7. Perry, J. J., Stiell, I. G., Sivilotti, M. L., Bullard, M. J., Emond, M., Symington, C., Sutherland, J., Worster, A., Hohl, C., Lee, J. S., Eisenhauer, M. A., Mortensen, M., Mackey, D., Pauls, M., Lesiuk, H., & Wells, G. A. (2011). Sensitivity of computed tomography performed within six hours of onset of headache for diagnosis of subarachnoid haemorrhage: prospective cohort study. British Medical Journal (Clinical research ed.), 343, d4277. https://doi.org/10.1136/bmj.d4277
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