Pathological Brain CT Findings – Illustration

Pathological Brain CT Findings

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
Cite this article as: Murat Yazici, Turkey, "Pathological Brain CT Findings – Illustration," in International Emergency Medicine Education Project, November 18, 2020, https://iem-student.org/2020/11/18/pathological-brain-ct-findings-illustration/, date accessed: February 25, 2021

Immediate Management of Paediatric Traumatic Brain Injury

Traumatic brain injury (TBI) has been noted as a leading cause of death and disability in infants, children, and adolescence (Araki, Yokota and Morita, 2017). In the UK alone, it’s approximated 1.4 million individuals attend the emergency department (ED) with head injury, and of those, 33%-50% are children under the age of 15; on top of this, a fifth of those patients admitted have features suggesting skull fracture or brain damage – that’s no small figure (NICE, 2014)! The particular importance of TBI in the paediatric population is that the treatment and management approach differs to adults; this is largely due to the anatomical and physiological differences in children. Furthermore, neurological evaluation in children proves more complex. All in all, children are complicated, and it is of great importance that we are aware of these differences when a paediatric patient arrives at the ED with TBI presentations.

Why is the paediatric population at risk for TBIs?

To delve slightly deeper into physiology and anatomy, there are several reasons children are at high risk of acquiring serious injury from TBIs. The paediatric brain has higher plasticity and deformity. As such, their less rigid skulls and open sutures allow for greater shock absorbance and response to mechanical stresses (Ghajar and Hariri, 1992). This ‘shaking’ of the brain inside the skull can stretch and tear at blood vessels in the brain parenchyma, resulting in cerebral haemorrhage.

Children also have a larger head-to-body size ratio, making the probability of head involvement in injury consequently higher (in comparison to adults); the head is also relatively heavier in a child, making it more vulnerable (especially in injury caused by sudden acceleration).

Young children have weaker neck muscles on top of having relatively heavier heads. Ligaments in the neck are relied on for craniocervical stability more so than the vertebrae. Hence, not only are TBIs more likely, but craniocervical junction lesions can also result from traumatic injury.

How does TBI in children come about?

The common causes of TBI in the paediatric population varies with age (Araki, Yokota and Morita, 2017). Some of these causes can be seen in the table below, which has been adopted from Araki, Yokota, and Morita (2017).

Table 1 Injury characteristics according to age and development

How can TBI in children present?

  • History: dangerous mechanism of injury (e.g. road traffic accidents or fall from a height greater than 1 meter)
  • Glasgow Coma Scale (GCS) less than 15 (at 2 hours after injury)
  • Visible bleeding, bruise, swelling, laceration
  • Signs of base-of-skull fracture:
    •  ‘Panda’ eyes – haemotympanum
    • Battle’s sign – cerebrospinal fluid leakage from ear or nose
  • Seizure (ask about history of epilepsy)
  • Focal neurological deficit
  • Vomiting
  • Loss of consciousness
  • Amnesia lasting more than 5 minutes
  • Abnormal drowsiness 

Note some children won’t have any of these signs, but if there is any suspicion of possible TBI, it should be investigated further.

Immediate management

There are various causes to paediatric TBI – also subdivided into primary and secondary TBI. Primary TBI includes skull fractures and intracranial injury. Secondary TBI can be caused by diffuse cerebral swelling. Primary and secondary TBI will be managed similarly in initial treatment (i.e. in the ED). The goal of baseline treatment is to:

  1. maintain blood flow to the brain
  2. prevent ischaemia (and possible secondary injury)
  3. maintain homeostasis 

Analgesia, Sedation, Seizure Prophylaxis

A level of anaesthesia needs to be achieved to allow for invasive procedures, such as airway management and intracranial pressure (ICP) control. Normally opioids and benzodiazepines are using in combination for analgesia and sedation in children. Instances where a child presents with a severe TBI (defined as a ‘brain injury resulting in a loss of consciousness of greater than 6 hours and a Glasgow Coma Scale of 3 to 8’), a neuromuscular block is used to improve mechanical ventilation, stop shivering, and reduce metabolic demand.

Anticonvulsants have been used in children, in particular infants, as they have a lower seizure threshold. Risk factors for early onset of seizures in infants under the age of 2 include hypotension, child abuse, and a GCS of ≤ 8; note, all of which may occur as a result of, or preceding, a TBI! For severe paediatric TBI cases, immediate prophylactic administration of anticonvulsants has been recommended.

Maintaining Cerebral Perfusion

The gold standard to measure ICP is an external ventricular drain (EVD); which can be used not only to measure ICP but can also be opened to drain additional CSF to reduce ICP. An intraparenchymal intracranial pressure sensor is an immediate invasive method used to detect early increased ICP in children with TBI. Monitoring of both ICP and cerebral perfusion pressure (CPP) is considered standard practice in TBI management in both paediatric and adult populations, as it is associated with better outcomes.

CPP is the pressure gradient which allows for cerebral blood flow. If this pressure is not maintained, the brain will lose adequate blood flow (Ness-Cochinwala and Dwarakanathan, 2019). Elevated CPP can accelerate oedema and increase chances of secondary intracranial hypertension.

Cerebral Perfusion Pressure (CPP) = Mean Arterial Pressure (MAP) – Intracranial Pressure (ICP)

A CPP of around 40-60 mmHg (40-50mmHg in 0-5 year-olds and 50-60mmHg in 6-17 year-olds) is considered ideal. Achieving an adequate CPP can be done by increasing MAP or reducing ICP (using the above equation). Hence it is necessary to have a good understanding of what good target values for MAP and ICP are.

A good target value for MAP is the upper end of ‘normal’ for the child’s age. Reaching this can be done by using fluids (if fluid deficient) or by use of inotropes. The recommended ICP target is < 20mmHg (normal is between 5-15 mmHg and raised ICP is regarded as values over 20mmHg).

When thinking about ICP, it’s useful to remember a mass in the brain; a mass being possible haemorrhage or any other space-occupying lesion. In TBI, oedema is most prominent at around 24-72 hours post-injury. As a result of increased mass, the initial consequence is a displacement of cerebrospinal fluid (CSF) into the spinal cord. Following this, venous blood in the cranium will also be displaced.

If ICP is further elevated, herniation can result – which is serious and often fatal! Signs of uncal herniation can present as unilateral fixed and dilated pupil. Signs of raised ICP can include pupillary dilatation and series of responses known as the ‘Cushing’s Triad’: irregular, decreased respiration (due to impaired brainstem function), bradycardia, and systolic hypertension (widened pulse pressure). Cushing’s triad results from the response of the body to overcome increased ICP by increasing arterial pressure.

Using the Monroe-Kellie Doctrine as a guide, we can predict how to reduce ICP. One management is head positioning. Head-of-bed should be elevated to 30˚, with the head in mid-line position, to encourage cerebral venous drainage. The EVD can also be used to drain CSF.

Commonly, intravenous mannitol and hypertonic saline are used to manage intracranial hypertension in TBI. Mannitol is traditionally used at a dosage of 20% at 0.25-1.0 g/kg – this is repeatedly administered. The plasma osmolality of the patient needs to be kept a close eye on; it should be ≤ 310 mOsm/L. 3% NaCl can be used to raise sodium levels to 140-150 mEg/L – this is slightly higher than normal sodium levels as a higher blood osmolarity will pull water out of neurons and brain cells osmotically and reduce cerebral oedema (Kochanek et al., 2019). Mannitol works in the same manner, however, use with caution as mannitol, being an osmotic diuretic, can cause blood pressure drops and compromise CPP! In last-resort emergency cases, where ICP need to be immediately reduced, a decompressive craniotomy can be performed.

Intravascular Volume Status

Measuring the patient’s central venous pressure (CVP) is a good indicator of the child’s volume status; 4-10 mmHg have been used as target thresholds. Alternatively, you can also monitor urine output (>1mL/kg/hr), blood urea nitrogen, and serum creatinine. Low volume status should be corrected with a fluid bolus. If the patient’s volume status is normal or high, but they remain hypotensive, vasopressors may improve blood pressure. At all costs, hypotension must be avoided, as if can lead to reduced cerebral perfusion and lead to brain ischaemia; on the other end, hypertension can cause severe cerebral oedema and should also be kept an eye on.

Other considerations​ - There have been reports of pituitary dysfunction in 25% of paediatric TBIs (during the acute phase). Do consider this if the patient had refractory hypotension – keep ACTH deficiency in mind!

Ischaemia

Prevent hypoxia at all costs! Hypoxia goes hand-in-hand with cerebral vasodilation – and as we already know, this increases the pressure in the cranium. Additionally, with hypoxia, there will be ischaemia. A minimum haemoglobin target of 7.0 g/dl is advised in a severe paediatric TBI case.

Other considerations​ - Whilst we are on the blood topic, also take care to correct and control any coagulopathies.

Ventilation

At a Paediatric Glasgow Coma Scale (PGCS) of less than 8, airways must be secured with a tracheal tube and mechanical ventilation commenced. SpO2 should be maintained at greater than 92%.

Of course, hypercapnia (CO2 > 6 kPa) and hypocapnia (CO2 < 4 kPa) are both not ideal, and we should maintain paCO2 at 4.5 – 5.3 kPa. However, some sources have suggested a quick fix to reduce ICP is to acutely hyperventilate the patient (as low CO2 results in cerebral vasoconstriction) – it’s suggested that paCO2 can safely go as low as 2.67 kPa before ischaemia kicks in! Mild hyperventilation is recommended (3.9 – 4.6 kPa)(Araki, Yokota and Morita, 2017).

Decreasing Metabolic Demand of the Brain

Body Temperature

What we want is to prevent hyperthermia, as it increases cerebral metabolic demands. Normothermia (36.5˚C – 37.5˚C) can be maintained by use of cooling blankets or antipyretics. There has been debate on whether therapeutic hypothermia has shown any benefit. Some studies have shown that moderate hypothermia for up to 48 hours, followed by slow rewarming, has prevented rebound intracranial hypertension as well as decreased ICP, however, there have not been any confirmed functional outcomes or decreased mortality rates benefits of this method (Adelson et al., 2013; Hutchinson et al., 2008).

Glycaemic control

Persistent hyperglycaemia (glucose > 10 mmol/L) should be treated. Hypoglycaemia (< 4 mmol/L) is much more dangerous. Persistent hyperglycaemia can be managed by reducing the dextrose concentration in IVF (which is usually administered in the first 48 hours of ICU care), or by starting an insulin drip.

A comment on imaging methods

In the UK, the initial investigation choice for detecting acute brain injuries is a CT head scan. A CT scan should be done within an hour of suspected head injury.
If there are no indications for a CT head scan (i.e. the signs/symptoms listed previously), a CT head scan should be performed within 8 hours of injury (NICE, 2014).

MRI scans are not usually done as the initial investigation, however, they have shown to provide information on the patient’s prognosis.

A final and most important note:

Don’t ever forget Safeguarding in children. Unfortunately, child maltreatment is common and can present anywhere. Have a look at the NICE guidelines below for more on how to identify child maltreatment.

Further reading

References

  • Adelson PD, Wisniewski SR, Beca J, Brown SD, Bell M, Muizelaar JP, Okada P, Beers SR, Balasubramani GK, Hirtz D; Paediatric Traumatic Brain Injury Consortium. Comparison of hypothermia and normothermia after severe traumatic brain injury in children (Cool Kids): a phase 3, randomised controlled trial. Lancet Neurol. 2013 Jun;12(6):546-53. doi: 10.1016/S1474-4422(13)70077-2.
  • Araki T, Yokota H, Morita A. Pediatric Traumatic Brain Injury: Characteristic Features, Diagnosis, and Management. Neurol Med Chir (Tokyo). 2017;57(2):82-93. doi:10.2176/nmc.ra.2016-0191
  • Finnegan R, Kehoe J, McMahon O, Donoghue V, Crimmins D, Caird J, Murphy J. Primary External Ventricular Drains in the Management of Open Myelomeningocele Repairs in the Neonatal Setting in Ireland. Ir Med J. 2019 May 9;112(5):930.
  • Ghajar J, Hariri RJ. Management of pediatric head injury. Pediatr Clin North Am. 1992;39(5):1093-1125. doi:10.1016/s0031-3955(16)38409-7
  • Hutchison JS, Ward RE, Lacroix J, Hébert PC, Barnes MA, Bohn DJ, Dirks PB, Doucette S, Fergusson D, Gottesman R, Joffe AR, Kirpalani HM, Meyer PG, Morris KP, Moher D, Singh RN, Skippen PW; Hypothermia Pediatric Head Injury Trial Investigators and the Canadian Critical Care Trials Group. Hypothermia therapy after traumatic brain injury in children. N Engl J Med. 2008 Jun 5;358(23):2447-56. doi: 10.1056/NEJMoa0706930.
  • Kochanek PM, Tasker RC, Bell MJ, Adelson PD, Carney N, Vavilala MS, Selden NR, Bratton SL, Grant GA, Kissoon N, Reuter-Rice KE, Wainwright MS. Management of Pediatric Severe Traumatic Brain Injury: 2019 Consensus and Guidelines-Based Algorithm for First and Second Tier Therapies. Pediatr Crit Care Med. 2019 Mar;20(3):269-279. doi: 10.1097/PCC.0000000000001737.
  • National Institute for Health and Care Excellence. Head injury: assessment and early management. 2014. Available at: https://www.nice.org.uk/guidance/cg176
  • Ness-Cochinwala M., Dwarakanathan D. Protecting #1 – Neuroprotective Strategies For Traumatic Brain Injury. Paediatric FOAMed. 2019. 
Cite this article as: Nadine Schottler, Great Britain, "Immediate Management of Paediatric Traumatic Brain Injury," in International Emergency Medicine Education Project, November 16, 2020, https://iem-student.org/2020/11/16/paediatric-traumatic-brain-injury/, date accessed: February 25, 2021

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Question Of The Day #21

question of the day
qod21

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

This patient experienced a witnessed cardiac arrest at home, after which pre-hospital providers initiated cardiopulmonary resuscitation (CPR, or “chest compressions”) and Advanced Cardiovascular Life Support (ACLS). ACLS includes the tenets of Basic Life Support (BLS), such as early initiation of high-quality CPR at a rate of 100-120 compressions/minute, compressing the chest to a depth of 5 cm (2 inches), providing 2 rescue breaths after every 30 compressions (30:2 ratio), avoiding interruptions to CPR, and allowing for adequate chest recoil after each compression. In the ACLS algorithm, intravenous epinephrine is administered every 3-5 minutes and a “pulse check” is performed after every 2 minutes of CPR. The patient’s cardiac rhythm, along with the clinical history, helps decide if the patient should receive defibrillation (“electrical shock”) or additional medications. The ACLS algorithm divides management into patients with pulseless ventricular tachycardia (pVT) or ventricular fibrillation (VF) and patients with pulseless electric activity (PEA) or asystole.

The cardiac rhythm seen during the pulse check for this patient is a wide complex tachycardia with a regular rhythm. In the setting of cardiac arrest, chest pain prior to collapse, and a history of acute coronary syndrome, ventricular tachycardia is the most likely cause. The ACLS algorithm advises unsynchronized cardioversion at 150-200 Joules for patients with pVT or VF. Watching the cardiac monitor for a rhythm change (Choice A) or checking for a pulse (Choice D) are not recommended after defibrillation. A major priority of both BLS and ACLS is to avoid interruptions to CPR, so the best next step in management is to continue CPR (Choice B) after defibrillation. Administration of intravenous adrenaline (Choice C) is helpful for cardiac arrests to initiate shockable rhythm and should be repeated every 3-5 minute or every 2 cycle of CPR, particularly valuable in asystole patients. Calcium gluconate is another drug that can be used in patients with hyperkalemia and indicated in a patient with known kidney disease, missed hemodialysis sessions, or a history of usage of medications that can cause hyperkalemia. Magnesium can be used for patients who show polymorphic VT, particularly Torsades de Pointes. The next best step in this scenario is to continue CPR, regardless of the etiology of the cardiac arrest. Correct Answer: B.

References

Cite this article as: Joseph Ciano, USA, "Question Of The Day #21," in International Emergency Medicine Education Project, November 13, 2020, https://iem-student.org/2020/11/13/question-of-the-day-21/, date accessed: February 25, 2021

Push Th(d)ose Vasopressors

Push Th(d)ose Vasopressors

Background

Since Scott Weingart first advocated for using push-dose pressors in the Emergency Department (ED) over a decade ago(1), push-dose vasopressors, also known as bolus-dose vasopressors have seemingly found their way into many EDs. However, recent studies have sought to ask more questions regarding its use and safety in the Emergency Department.

Vasopressors such as epinephrine and norepinephrine are commonly used for regulating and maintaining adequate blood pressure or mean arterial pressure (MAP). While these are usually administered as a continuous infusion via central access, administering them as a small bolus through peripheral access came to be known as push-dose vasopressor in practice.

Traditionally, this small bolus strategy was used in the operating room (OR) by anesthetists to treat transient hypotension due to sedating agents or spinal anesthesia. Multiple studies have supported the safety and efficacy of push-dose vasopressors in this clinical setting/patient population (2).

Swensen, et al. (3) studied the safety of bolus-dose phenylephrine for hypotension in the Emergency Department, however, data on the efficacy and safety of push-dose pressors remains sparse in ED and in-patient settings. Studies published in the past few years have questioned the lack of evidence regarding the safety and efficacy of push-dose pressor use in ED settings and highlighted some negative consequences of its use (4). To understand the concerns, it’s important we first understand the vasopressors, indications for use, and preparation in the ED.

Push-dose pressors in the Emergency Department

The two common vasopressors used as push-dose pressors in the Emergency Department are Epinephrine and Phenylephrine. Patients needing emergency airway, traumatic brain injury, and post-cardiac arrest with the return of spontaneous circulation may all experience hypotension which could lead to adverse outcomes. Push-does pressors have been proposed as a temporary measure to limit the hypotension while a vasopressor infusion/definitive treatment is being set up (5).

phenilephrine vs epinephrine
push dose epinephrine
push dose phenilephrine

Clinical settings in the ED where the use of push-dose pressor is proposed:

  1. Airway management: Hypotension prior, during, and post-intubation could be treated with bolus-dose vasopressors. Panchal et al. (6) did a retrospective chart review of intubated hypotensive patients in which phenylephrine was used. Bolus-dose phenylephrine demonstrated an increase in systolic blood pressure and the authors recommended further studies to understand the best use of phenylephrine for post-intubation hypotension.
  2. Return of spontaneous circulation (ROSC): In patients with ROSC, bolus-dose pressors may aid in the maintenance of end-organ perfusion, which is often impaired after ROSC (7).
  3. Traumatic brain injury: By rapidly increasing mean arterial pressure and thus cerebral perfusion pressure, bolus-dose vasopressors may help to prevent secondary brain injury.

What are the concerns regarding the use of push-dose pressors in the ED?

Acquisto and Bodkin (8) cited a few dosing errors while using push-dose pressors and highlighted that emergency physicians are less familiar with the practice of medication preparation/manipulation and hence dosing errors are expected, inadvertently causing patients more harm than benefit. They also emphasized on the lack of evidence in the literature regarding the efficacy and safety of push-dose pressors in a stressful environment like the ED.

Rotando and Picard et al. (9) in their prospective observational study of 146 patients receiving push-dose pressors in the ICU had thirteen (11.2%) patients have a dose-related medication error and seventeen (11.6%) adverse events. They concluded while push-dose pressors where efficacious, they were associated with adverse drug events and medication errors.

Cole et al (10). performed a retrospective analysis of 249 patients receiving push-dose pressors and found a higher incidence of adverse hemodynamic effects (39%) and human errors (19%). They emphasized the need for further studies to question whether push-dose pressors improve outcomes, and if so, how to safely implement them in practice.

Another concern raised is whether physicians may bypass standard resuscitation practices of fluid boluses in favor of using push-dose pressors. Schwartz et al. (11) found that only 34% of patients received an appropriate fluid challenge before using push-dose pressors in a retrospective chart review of 73 patients receiving push-dose pressors for acute hypotension in the ED. Furthermore, it appeared that patients who did not receive an appropriate fluid bolus needed more doses of bolus-dose pressors followed by the need for continuous vasopressor infusion within 30 minutes of bolus-dose pressor use.

Emergency physicians work in stressful environments which raises concerns on the ability of the physician to perform accurate dose calculations under duress (4). The prepared syringe also contains multiple individual doses, and using more concentrated solutions potentially increases the risk of overdose and extravasation injury (12).

Conclusion

While the practice of using push-dose pressors has found its way into the Emergency Department, it is crucial to acknowledge that evidence regarding its safety and benefits is limited. However, rather than disregarding the practice, high-quality research should be encouraged, which could potentially be practice-changing. Holden et al. (12) offer a framework of operational and safety considerations for the use of push-dose pressors in the ED and is a must-read for all using push-dose pressors in their current practice.

References

  1. Scott Weingart. EMCrit Podcast 6 – Push-Dose Pressors. EMCrit Blog. Published on July 10, 2009. Accessed on September 25th 2020. Available at [https://emcrit.org/emcrit/bolus-dose-pressors/ ].
  2. Lee A, Ngan Kee WD, Gin T. A quantitative, systematic review of randomized controlled trials of ephedrine versus phenylephrine for the management of hypotension during spinal anesthesia for cesarean delivery. Anesth Analg. 2002 Apr;94(4):920-6, table of contents. doi: 10.1097/00000539-200204000-00028. PMID: 11916798.
  3. Swenson K, Rankin S, Daconti L, Villarreal T, Langsjoen J, Braude D. Safety of bolus-dose phenylephrine for hypotensive emergency department patients. Am J Emerg Med. 2018 Oct;36(10):1802-1806. doi: 10.1016/j.ajem.2018.01.095. Epub 2018 Feb 19. PMID: 29472039.
  4. Cole JB. Bolus-Dose Vasopressors in the Emergency Department: First, Do No Harm; Second, More Evidence Is Needed. Ann Emerg Med. 2018 Jan;71(1):93-95. doi: 10.1016/j.annemergmed.2017.05.039. Epub 2017 Jul 26. PMID: 28754354.
  5. Weingart S. Push-dose pressors for immediate blood pressure control. Clin Exp Emerg Med. 2015;2(2):131-132. Published 2015 Jun 30. doi:10.15441/ceem.15.010
  6. Panchal AR, Satyanarayan A, Bahadir JD, Hays D, Mosier J. Efficacy of Bolus-dose Phenylephrine for Peri-intubation Hypotension. J Emerg Med. 2015 Oct;49(4):488-94. doi: 10.1016/j.jemermed.2015.04.033. Epub 2015 Jun 20. PMID: 26104846.
  7. Gottlieb M. Bolus dose of epinephrine for refractory post-arrest hypotension. CJEM. 2018 Oct;20(S2):S9-S13. doi: 10.1017/cem.2016.409. Epub 2017 Jan 10. PMID: 28069098.
  8. Acquisto NM, Bodkin RP, Johnstone C. Medication errors with push dose pressors in the emergency department and intensive care units. Am J Emerg Med. 2017 Dec;35(12):1964-1965. doi: 10.1016/j.ajem.2017.06.013. Epub 2017 Jun 7. PMID: 28625533.
  9. Rotando A, Picard L, Delibert S, Chase K, Jones CMC, Acquisto NM. Push dose pressors: Experience in critically ill patients outside of the operating room. Am J Emerg Med. 2019 Mar;37(3):494-498. doi: 10.1016/j.ajem.2018.12.001. Epub 2018 Dec 3. PMID: 30553634.
  10. Cole JB, Knack SK, Karl ER, Horton GB, Satpathy R, Driver BE. Human Errors and Adverse Hemodynamic Events Related to “Push Dose Pressors” in the Emergency Department. J Med Toxicol. 2019 Oct;15(4):276-286. doi: 10.1007/s13181-019-00716-z. Epub 2019 Jul 3. PMID: 31270748; PMCID: PMC6825064.
  11. Schwartz MB, Ferreira JA, Aaronson PM. The impact of push-dose phenylephrine use on subsequent preload expansion in the ED setting. Am J Emerg Med. 2016 Dec;34(12):2419-2422. doi: 10.1016/j.ajem.2016.09.041. Epub 2016 Sep 22. PMID: 27720568.
  12. Holden D, Ramich J, Timm E, Pauze D, Lesar T. Safety Considerations and Guideline-Based Safe Use Recommendations for “Bolus-Dose” Vasopressors in the Emergency Department. Ann Emerg Med. 2018 Jan;71(1):83-92. doi: 10.1016/j.annemergmed.2017.04.021. PMID: 28601272.
Cite this article as: Neha Hudlikar, UAE, "Push Th(d)ose Vasopressors," in International Emergency Medicine Education Project, November 11, 2020, https://iem-student.org/2020/11/11/push-thdose-vasopressors/, date accessed: February 25, 2021

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Hypoglycemia – A Rural Perspective

hypoglycemia - a rural perspective

Waiting for patients is among some of the weird perks of working in a rural ER. “Too little isn’t fun as well”, said an enthusiastic new paramedic at Beltar PHC. Later that night, I’d find a funny connection between what he said and what followed.

A 56Y/M patient is brought to the ER on a particularly silent evening. Following the usual ER premise; I reach the department from upstairs. The patient was unconscious when I arrived. A paramedic was trying to open a peripheral line, and a nurse was taking a pulse oximeter reading while keeping the patient at 2L via nasal cannula. The bystanders who brought him had no clue of what had happened or if the patient had any comorbidity. As I grabbed the glucometer from the drawer, I could not help but remember how in med school exams all the hypoglycemic patients were medics who injected themselves with insulin. As I poked the patient with a lancet and measured his blood glucose, I realized the paramedic had already given up trying to get IV access. “I couldn’t get in”, he said. The glucometer beeped exactly then as if to confirm “this is trouble” – 37! “That is hypoglycemia”, I exclaimed!

Although there is no universally accepted definition of hypoglycemia (low blood glucose), a level below 60 rings the bell. As I tried to establish the line, I requested my nurse to prepare a thick paste of glucose powder. Of all the medicine I was taught, one thing I’ve found the most useful is the “available” medicine. Sure, start with a bolus of the glucose-containing solution: D50 or D10, if you cannot get IV access go for IM glucagon and so forth. But when you’re working in a setting where you second guess yourself for wasting a lancet while checking a patient’s blood glucose, IM glucagon becomes nothing more than a very good test question.

I could not get the line started either. Minutes after we applied the glucose paste on the buccal mucosa, the patient woke up. The sigh of relief was audible in the small ER of our PHC. Eventually, we were able to feed the patient per oral. The patient turned out to be diabetic who thought, “insulin is a medicine, hence should not be ignored, but the food is optional.”

Clinical hypoglycemia is sometimes defined as blood glucose low enough to cause symptoms. For most people, this occurs at 50-60 mg/dL. Clinically significant hypoglycemia is confirmed by the presence of the ‘Whipple triad’. Yap, that’s the same Allen Whipple, the American surgeon who also coined the Whipple procedure! The presence of symptoms consistent with hypoglycemia, a low serum glucose level, and resolution of the symptoms and signs of hypoglycemia with the administration of glucose is what confirms hypoglycemia.

Because diabetics are most prone to get hypoglycemic, in a diabetic patient, hypoglycemia is defined as a self-monitored blood glucose level ≤ 70mg/dL. Everyone else must have a documented experience of Whipple’s triad for the diagnosis. There is also something called relative hypoglycemia, it occurs when a patient with diabetes reports hypoglycemic symptoms, but the blood glucose remains above 70 mg/dL. This still requires treatment. Remember, we treat patients, not numbers.

The causes of hypoglycemia can be diverse, but the horses include missed meals or overnight fasting but still using hypoglycemic agents (sulphonylureas, insulin) in a person with diabetes. Be vigilant about recent exercise enthusiasts, alcohol ingestion, weight loss, and renal failure (which can reduce insulin clearance).

Signs and symptoms of hypoglycemia in non-diabetic patients are generally fairly obvious. Sympathetic autonomic nervous system activation symptoms like nervousness, anxiety, tremulousness, sweating, palpitations, shaking, dizziness, hunger, and symptoms due to decreased availability of glucose to the brain; confusion, weakness, drowsiness, speech difficulty, incoordination, odd behavior are seen below the commonly quoted glycemic values of 50-60. In severe cases, hypoglycemia may result in seizures, coma, or death.

A logical treatment flowchart should start with a glucose-containing solution: D50 or D10. In regards to D50, be aware that the bolus may cause rebound hypoglycemia, may overshoot glycemic targets and is hypertonic hence should be given slowly over 2-5 minutes. There has been extensive debate over D50 vs D10, here is what I try to keep in mind; If using D50, give 1 amp at a time over 2-5 mins. If D10, a 100ml bolus over 2 mins. Check the patients’ glucose levels often.

Remember both of those approaches require you to have IV access. Intramuscular glucagon (5mg) may be given to raise serum glucose levels. Keep in mind two things: the efficacy of glucagon is dependent upon hepatic glycogen stores. Patients with prolonged hypoglycemia may have a minimal response and repeating glucagon does not make much sense.

If the blood glucose goes back to > 60mg/dL in a non-diabetic patient, and >70mg/dL in a diabetic patient and/or there is an improvement in symptoms, patients who can eat should do so otherwise IV dextrose drip (D5W at 75-100 mL/hr) is the way to go.

Cite this article as: Carmina Shrestha, Nepal, "Hypoglycemia – A Rural Perspective," in International Emergency Medicine Education Project, November 9, 2020, https://iem-student.org/2020/11/09/hypoglycemia-a-rural-perspective/, date accessed: February 25, 2021

Read Other Posts from Dr. Shrestha

Question Of The Day #20

question of the day
cod20
608 - Figure3 - pericardial effusion - ECG

Which of the following is the most appropriate next investigation for this patient’s condition?

This patient’s EKG demonstrates alternating amplitudes of QRS complexes, a phenomenon known as electrical alternans. This is caused by the heart swinging back and forth within a large pericardial effusion. The patient is tachycardic and borderline hypotensive, which should raise concern over impending cardiac tamponade. The next best investigation to definitively diagnose a large pericardial effusion with possible tamponade would be a cardiac sonogram (Choice B). This investigation could also guide treatment with pericardiocentesis in the event of hemodynamic decompensation and the development of obstructive shock. Other EKG signs of a large pericardial effusion are diffusely low QRS voltages and sinus tachycardia. Chest radiography (Choice C) may show an enlarged cardiac silhouette in this case and evaluate for alternative diagnoses (i.e. pneumothorax, pleural effusions, pneumonia, atelectasis), however, cardiac echocardiography is the best next investigation. CT pulmonary angiography (Choice D) would demonstrate the presence of a pericardial effusion along with differences in cardiac chamber size indicative of tamponade. Still, bedside cardiac sonogram is a faster test that prevents a delay in diagnosis. Sending a potentially unstable patient for a CT scan may also be dangerous. Arterial blood gas testing (Choice A) has no role in diagnosing pericardial effusion or cardiac tamponade. Correct Answer: B

References

Cite this article as: Joseph Ciano, USA, "Question Of The Day #20," in International Emergency Medicine Education Project, November 6, 2020, https://iem-student.org/2020/11/06/question-of-the-day-20/, date accessed: February 25, 2021

Approach to Acute Cough in Adults

Approach to Acute Cough in Adults

Cough is one of the most common complaints presenting to any emergency physician or primary care practitioner – whether it is the chief complaint or an associated symptom. An acute cough is one that has been present for less than three weeks. In the era of COVID-19, a patient presenting with an acute cough can be alarming and scary. So, now more than ever, it is important to develop a strong diagnostic approach to the acute cough, which is largely a clinical diagnosis.

Differential Diagnosis of Acute Cough

*Indicates the most common causes of acute cough.
Cause Example Symptoms / warning signs
Infectious (viral/bacterial) Upper respiratory tract infection aka common cold* Rhinorrhea, nasal obstruction, sneezing, scratchy/sore throat, malaise, headache, and no signs of consolidation
Acute bronchitis* Recent upper respiratory tract infection, and absence of COPD, and absence of high fever or other systemic signs
Influenza Fever, sore throat, nasal congestion, myalgia, headache, and no signs of consolidation
Pneumonia* Fever, tachycardia, tachypnea, consolidation signs on respiratory exam, and mental status change in patients >75y old
Pertussis Whooping cough and cough-emesis
COVID-19 Fever, non-productive cough, fatigue, dyspnea, and/or other less common symptoms such as sore throat, diarrhea, headache, skin rash, and anosmia
Post-nasal drip aka upper airway cough syndrome Post-nasal drainage sensation, need to clear throat, and rhinorrhea

Allergic rhinitis aka hay fever Itching and watering of eyes, rhinorrhea, pruritis
Exacerbation of a pre-existing chronic disease Exacerbation of Asthma   History of episodic wheezing, non-productive cough, dyspnea, reversible air-flow obstruction, allergen exposure or triggered by exercise
Exacerbation of COPD Smoking history, dyspnea, signs of obstruction on respiratory exam i.e. decreased breath sounds, and irreversible air-flow obstruction
Exacerbation of CHF Dyspnea, orthopnea, peripheral edema, gallop rhythm on cardiac exam, and elevated JVP
Drug-induced ACE inhibitor use Non-productive cough, tickling or scratchy sensation in throat typically arising within 1 week of starting medication
Gastroesophageal reflux disorder (GERD)

 

Heartburn, regurgitation, dysphagia, and cough is more prominent at night
Other pulmonary causes Pulmonary embolism Clinical signs and symptoms of DVT, dyspnea, tachypnea, tachycardia, pleuritic chest pain, immobilization for 3 or more days, surgery in the past 4 weeks, history of DVT/PE, hemoptysis, and malignancy with active treatment in the past 6 months
Lung cancer Smoking history, new change in cough, hemoptysis, dyspnea, night sweats, weight loss, and signs of focal obstruction on respiratory exam i.e. decreased breath sounds
Foreign body aspiration Dyspnea, inspiratory stridor, choking, and elevated risk in children
Acute inhalation injury History of exposure to smoke (e.g. in firefighters, thermal burn victims) or chemicals (e.g. chlorine, ammonia)
Bronchiectasis Large volumes of purulent sputum, dyspnea, wheezing, and chest pain
Interstitial lung disease Non-productive cough, dyspnea, fatigue, weight loss
         

Picture the scene: A 23-year-old female presents to the emergency department with a cough that has been ongoing for one week. What are your next steps?

History

  1. Confirm the duration and timing of cough
  2. Nature of cough, i.e. whooping, hemoptysis, and productive vs non-productive?
  3. Presence of the following associated symptoms: fever, dyspnea, sore throat, headache, chest pain, heartburn, rhinorrhea, facial pressure/pain, nasal congestion, or weight loss
  4. History of any chronic lung disease (i.e. asthma, COPD), allergies, CHF, or immunosuppression?
  5. Smoking history?
  6. Medication history, i.e. ACE inhibitor use?

Physical Exam

  1. Vitals
  2. HEENT exam (head, eyes, ears, nose, and throat)
  3. Respiratory exam
  4. Cardiac exam, including JVP

Laboratory Tests

  • Send for COVID-19 swab according to your hospital’s guidelines
  • Order CBC if suspecting infection
  • Order ABG if dyspnea present or life-threatening cause of acute cough suspected
  • Order sputum culture if suspecting bacterial pneumonia
  • Spirometry if need to differentiate between obstructive lung disease (e.g., asthma, COPD) and restrictive lung disease (e.g., interstitial lung disease)

Imaging

  • Consider starting with a Chest X-ray if red flags for serious pathology are present >> dyspnea, hemoptysis, chest pain, weight loss, immunosuppression, significant smoking history, elderly or at risk of aspiration, tachypnea or hypoxemia, abnormal cardiac or respiratory exam, or sepsis.
  • If suspecting foreign body aspiration, need to order bronchoscopy 

Please note that treatment of the conditions that may cause acute cough are not discussed in this blog post, but can be found through medical resources such as those in the references section. Treatment for acute cough often requires treating the underlying cause.

References

  1. Boujaoude ZC, Pratter MR. Clinical approach to acute cough. Lung. 2010;188 Suppl 1(Suppl 1):S41-S46. doi:10.1007/s00408-009-9170-6
  2. Holzinger F, Beck S, Dini L, Stöter C, Heintze C. The diagnosis and treatment of acute cough in adults. Dtsch Arztebl Int. 2014;111(20):356-363. doi:10.3238/arztebl.2014.0356
  3. Madison JM, Irwin RS. Cough: A worldwide problem. Otolarynogol Clin North Am. 2010 Feb;43(1):1-13, vii.
  4. Strong Medicine. An Approach to Cough. Published 25 March, 2018. https://www.youtube.com/watch?v=LDMEtNXik-A
  5. University of Toronto. Cough and Dyspnea. 2015. http://thehub.utoronto.ca/family/cough-and-dyspnea/ Accessed 17 August, 2020.

 

Cite this article as: Sheza Qayyum, Canada, "Approach to Acute Cough in Adults," in International Emergency Medicine Education Project, November 4, 2020, https://iem-student.org/2020/11/04/approach-to-acute-cough-in-adults/, date accessed: February 25, 2021

From Missed Hemodialysis to Multiple Arrhythmias

From Missed Hemodialysis to Multiple Arrhythmias

Case Presentation

A 78-year-old male, known case of Chronic Kidney Disease on maintenance hemodialysis, presented to the Emergency Department with dizziness and lethargy complaints about 2 days. He had missed his last hemodialysis session due to personal reasons. We could not elicit any further history details as was significantly dyspneic (no bystanders with him at the time of presentation). Hence, the patient was received in Bay 1 for immediate resuscitative measures. The patient was afebrile, conscious, and well oriented, but unable to communicate because of severe dyspnea.

Vitals

HR – 142 beats/min
BP – not recordable
RR – 36 breaths/min
SpO2 – poor tracing, intermittently showed 98% on room air (15 LO2 via Non Rebreathing Mask was initiated nevertheless)

ECG

ECG on presentation
Monomorphic ventricular tachycardia

He was immediately connected to a defibrillator in anticipation of possible synchronized cardioversion. Simultaneously, the cause of the possible rhythm was being evaluated for and a thorough examination was carried out. On examination, his lung fields were clear. His left arm AV Fistula had a feeble thrill on palpation.

In suspicion of hyperkalemia as the cause of VT, patient was immediately started on potassium reduction measures while the point of care ABG report was awaited. He was treated with salbutamol nebulization 10mg, sodium bicarbonate 50 ml IV and 10% calcium gluconate 10ml IV. In view of hemodynamic instability, he was also started on intravenous noradrenaline infusion.

ABG Findings

pH – 7.010, pCO2 – 20.8 mmHg, pO2 – 125 mmHg, HCO3 – 7 mmol/L, Na – 126 mmol/L, K – 9.6 mmol/L

As hyperkalemia was confirmed, the patient was also given 200 ml of 25% dextrose with 12 units of Rapid-acting insulin IV. With the above measures, the patient’s cardiac rhythm came to a sine wave pattern. 

He was later taken up for emergency hemodialysis (HD) – Sustained Low Efficacy Dialysis (SLED) in the ICU, using a low potassium dialysate. Since his AV fistula was non-functioning, HD was done after placement of a femoral dialysis catheter. 2 hours into HD, the patient’s cardiac monitor showed a normal sinus rhythm. His hemodynamic status significantly improved. Noradrenaline infusion was gradually tapered and stopped by the end of the HD session, and repeat blood gas analysis and serum electrolytes showed improvement of all parameters. 

after hemodialysis

The patient was discharged 2 days later, after another session of hemodialysis (through AV fistula) and a detailed cardiology evaluation (ECHO – LVH, normal EF).

For the Inquisitive Minds

  1. The patient underwent a detailed POCUS evaluation, both in the ER and ICU. What findings do you expect to find on the RUSH examination for this patient?
  2. His previous ECHO report (done 1 month ago) mentioned left ventricular hypertrophy and normal ejection fraction. So what would be the reason behind the POCUS findings? Is it reversible?
  3. Why was the AV fistula non-functioning at the time of presentation? When would it have started to function again?
  4. Despite not having hypoxia, this patient was given supplemental oxygen. Did he really require it, and if so, what was the rationale?
  5. What was the necessity for carrying out SLED for this patient?
  6. Why was this patient not immediately cardioverted in the ER?
  7. If this patient had gone into cardiac arrest, what drugs would you have given for management of hyperkalemia?
  8. How differently would you have managed this patient?

Please give your answers and comments into "leave a reply" area below.

Cite this article as: Gayatri Lekshmi Madhavan, India, "From Missed Hemodialysis to Multiple Arrhythmias," in International Emergency Medicine Education Project, November 2, 2020, https://iem-student.org/2020/11/02/missed-hemodialysis/, date accessed: February 25, 2021
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Question Of The Day #19

question of the day
qod19
52 - Perforated Viscus

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

All patients who present to the emergency department with chest pain should be evaluated for the top life-threatening conditions causing chest pain. Some of these include myocardial infarction, pulmonary embolism, esophageal rupture, tension pneumothorax, cardiac tamponade, and aortic dissection. Many of these diagnoses can be ruled-out or deemed less likely with a detailed history, physical exam, EKG, and sometimes imaging and blood testing. This patient presents with vague, burning chest pain, nausea, and tachycardia on exam. Pulmonary embolism (Choice A) is hinted by the patient’s tachycardia, but the patient has no tachypnea or risk factors mentioned for PE. Additionally, the chest X-ray findings demonstrate an abnormality that can explain the patient’s symptoms. Pancreatitis (Choice B) and Gastroesophageal reflux disorder (Choice D) are also possible diagnoses, especially with the location and description of the patient’s pain. However, Chest X-ray imaging offers an explanation for the patient’s symptoms. The patient’s Chest X-ray demonstrates the presence of pneumoperitoneum. In the presence of NSAID use, this radiological finding raises concern over a perforated viscus from advanced peptic ulcer disease (Choice C). Peptic ulcer disease (PUD) is most commonly caused by Helicobacter pylori infection, but NSAIDs, iron supplements, alcohol, cocaine, corrosive substance ingestions, and local infections can cause PUD. PUD is a clinical diagnosis which can be confirmed visually via endoscopy. The treatment for PUD includes initiation of a proton pump inhibitor (H2-receptor blockers are 2nd line), avoiding the inciting agent, and H.pylori antibiotic regimens in confirmed H.pylori cases. The treatment for a perforated peptic ulcer with pneumoperitoneum is IV fluids, IV antibiotics, Nasogastric tube placement, and surgical consultation for repair.

References

Cite this article as: Joseph Ciano, USA, "Question Of The Day #19," in International Emergency Medicine Education Project, October 30, 2020, https://iem-student.org/2020/10/30/question-of-the-day-18-2/, date accessed: February 25, 2021

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The EKG Case of No Symptoms

the ecg case of no symptoms

Case Presentation

A 52-year-old woman presents to the ED from an outpatient dialysis center with a rather vague history. She has no symptoms and feels normal, but she was told something “was either too low or too high” on her vital signs at dialysis, so dialysis staff did not perform her scheduled dialysis session. No one had called ahead to alert the emergency department, and the patient had driven herself to the ED, as she was instructed. Vitals show a normal temperature, respiratory rate, oxygen saturation, blood pressure of 102/47 mm Hg, and a heart rate of 138 beats per minute. The physical exam is normal besides a mild regular tachycardia and a working AV dialysis fistula on the right arm. EKG is done, and a representative portion is shown below:

EKG from the prior year is shown for comparison.

How would you interpret the first EKG, and what are your next steps?

Discussion

While you are thinking, I will discuss a few of my practical observations from working in the pit. I want to focus not so much on the diagnosis but on working with these types of scenarios.

Treat the patient and not the chief complaint, vitals, labs, EKGs, studies, or referral information.

When they are feeling great and have no symptoms, they are feeling great and have no symptoms! Your nurses will not necessarily think this way, but one does not feel great while having a real STEMI apparent on the triage EKG. So what is it then, if the patient is here for a contact lens stuck in their eye, but has an EKG STEMI? Worst case – a prior STEMI that never corrected or evolved on the EKG. A ventricular aneurysm? Leads misplaced? Did your EKG tech do an EKG on themselves? A silent MI can occur, but an incidental STEMI is unlikely. 

Of course, the patient has to be alert, competent, and not intoxicated. They should not be lying about or hiding their symptoms and should not have a secondary interest like the need to make it to a daughter’s wedding - live or die. The easiest thing is to ask directly.

What is the rhythm's rate doing when it is left alone?

Afibs and MATs will tend to vary greatly in the second to second heart rate, sinus tachycardias will fluctuate some, while A-flutters and SVTs will tend to stick to a single number no matter what you do and no matter if the patient is walking, talking, or snoozing. Stable Vtachs will depend on a number of factors like being monomorphic or polymorphic – but we are talking about narrow QRS dysrhythmias or ones with an obvious bundle. 

So if you cannot tell from the EKG – observe what the thing does while left alone. As long as the patient is otherwise stable or has had symptoms for a while, you have some time.

Adenosine – not just for SVT conversion

“SVT = adenosine” should not be an automatic equation. First of all, there are contraindications to adenosine based on past history or current medications taken. But adenosine can also be used to “stretch out” weird or equivocal fast rhythms to make flutter waves or hidden P waves come out, so you can see and diagnose the arrhythmia vs. sinus. 

You have to have continuous EKG recording going or printing the monitor strip to spot the temporary effect.

Hypotension + tachy-dysrhythmia: does not necessarily add up to Joules.

The textbook mantra of shocking any dysrhythmia associated with hypotension does not hold up in reality. In reality, you will find that most of your Afibs with a rapid response, your new-onset atrial flutters and your SVTs will have a lousy blood pressure: systolic of 80s and 90s are almost to be expected, and may even dip down to 70s on occasion. It also depends on a prior BP baseline, if the person is petite or dehydrated. But if the patient is mentating well and is not suffocating or experiencing crushing chest pain with diaphoresis, please don’t feel like you have to shock them. The body is not used to the new arrhythmia, and the rapid rate compromises the cardiac output. 

Yes, you can still use your rate and rhythm controllers. Give the patient a gentle fluid bolus if you must. Of course, pacer pads do have to be on ahead of time.

Be afraid of shocking dialysis patients. Check electrolytes.

Hypotension with normal mentation is much better than a PEA arrest. Shocking extremes of electrolyte and acid/base abnormalities, whether due to TCA and other overdoses or in dialysis patients, will give you exactly that. This is especially true for the so-called “slow-X” arrhythmias: slow Afib, slow SVT, or even V-slow (Vtach with a rate of 130) that dialysis patients like to present in. 

Just like airplane travel in transportation, electricity is in general the safest rhythm conversion strategy. But there are exceptions, and you only need to crash once.

A-flutter and the stuck rate of 150

You already know this, but just as a reminder. If the rate is a steady 150, plus or minus, and it is stuck there, you should think of atrial flutter. 

Even if you do not see obvious classic flutter waves, there is a high chance of 2:1 conduction. In this case, I thought of it. Fortunately, it did not think of me.

Adenosine (again)….the 6, the 12…the 24??

Sometimes adenosine is not pushed correctly, but sometimes it just does not work or only works for a few seconds. Sometimes the patient’s Mom knows best what works, so you should listen. Sometimes the last time it was used, the patient really did feel like they were going to die – so they do not ever want it again. Ever. That you should try 6mg, then 12mg, then stop is generally true, but it is also a dead-end. What is your back up plan? Electricity? In the past I have given the doses in reverse, combined 6mg with the Valsalva maneuver and had given a preemptive beta-blocker or calcium channel blocker dose 10-15 minutes before adenosine to massage a stubborn heart into adenosine submission. It is ok to experiment a little. Another practical point – how much does your ED freak an SVT patient out while he or she is being triaged and roomed? I still do not completely understand why an SVT tends to be rushed up in the same fashion as a STEMI with cardiogenic shock and bradycardia, judging from staff adrenaline levels. 

Calm the patient down, turn the lights off and let them change. It's like a kid with croup. Remember, it is lack of the sympathetic influx that we want, not an excess. Otherwise, why try the Valsalva at all? Has anyone attempted a stellate ganglion block Vfib-style for a refractory SVT? An overkill, I know….but could be fun, and practice for the real deal.

Aren’t all AVNRTs verapamil sensitive?

Years ago, in my first year of solo practice, I had a case of a refractory SVT in a young teenager, which a pediatric cardiologist consulting by phone called a “verapamil-sensitive AVNRT” based on the EKG alone. I was impressed. Hours later, I decided to flash my newly acquired cool knowledge and relayed the same to my in-house cardiologist, who looked at me with a grin and a raised eyebrow and said, “Anthony, all AVNRTs are verapamil sensitive”. At that time, I was also sensitive, and so my feelings were hurt. Lately I have gotten into the habit of treating my SVTs with diltiazem – as a purer verapamil relative. With generally good results and no need to stand in front of the patient during administration by the nurse. 

The bottom line is – you have choices. Especially, if the patient is already on a beta-blocker or a calcium channel blocker, give them a beta or a calcium blocker IV, see what happens.

Case Concluded

Despite a single nadir of blood pressure of 75 systolic, the rest holding steadily in the high 90s, the patient received a single dose of IV diltiazem and a small IV fluid bolus. Labs reviewed prior showed normal potassium, calcium, sodium, magnesium and the rest of them. Her average heart rate reduced to about 106 and a repeat EKG is shown, accidentally capturing an event: 

She, of course, had a “verapamil sensitive” SVT. The patient’s new right bundle block had also improved to an incomplete, proving to be either SVT- or rate-related. The patient had never experienced any symptoms while in the ED. She was observed for a short time, scheduled for an out-of-sequence dialysis the next day and discharged home with a normal heart rate. I guess, in this case, we did treat the EKG and not the patient.

Cite this article as: Anthony Rodigin, USA, "The EKG Case of No Symptoms," in International Emergency Medicine Education Project, October 26, 2020, https://iem-student.org/2020/10/26/the-ekg-case-of-no-symptoms/, date accessed: February 25, 2021

Want to read more, take a look this post from September

Question Of The Day #18

question of the day
qod18
839 - diffuse ST elevation - pericarditis?

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

This patient presents to the emergency department with signs and symptoms consistent with acute pericarditis from a likely viral etiology. Common causes of acute pericarditis include idiopathic, infectious (viral, bacterial, or fungal), malignancy, drug-induced, rheumatic disease-associated (lupus, rheumatoid arthritis, etc.), radiation, post-MI (Dressler’s Syndrome), uremia, and severe hypothyroidism. The chest pain associated with this diagnosis is typically worse with supine positioning, improved with sitting forward, worse with inspiration, and may radiate to the back. A pericardial friction rub may be heard on auscultation of the chest, and there may be a low-grade fever on the exam. The hallmark EKG demonstrates diffuse ST-segment elevation with PR segment depression, although normal ST segments or T wave inversions can be seen on EKG later in the disease process. The treatment of acute pericarditis depends on the underlying cause of the disease. This patient has likely viral pericarditis with no clinical signs of myocarditis (i.e. fluid overload, cardiogenic shock, etc.) or cardiac tamponade (i.e. obstructive shock, distended neck veins, muffled heart sounds, low voltage QRS complexes or electrical alternans on EKG). A cardiac sonogram would be prudent to evaluate for a pericardial effusion. This patient’s disease course likely will resolve with NSAIDs in 1-2 weeks. Ibuprofen (Choice C) is the preferred treatment over aspirin (Choice A) or steroids (Choice B). Colchicine (Choice D) can be useful in recurrent episodes of pericarditis to reduce recurrence and in acute pericarditis not responding to NSAIDs. Correct Answer: C 

References

Cite this article as: Joseph Ciano, USA, "Question Of The Day #18," in International Emergency Medicine Education Project, October 23, 2020, https://iem-student.org/2020/10/23/question-of-the-day-18/, date accessed: February 25, 2021

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Suicide – An Emergency Priority of Public Health Care

Suicide An Emergency

A significant number of emergency department visits annually arise as a result of intentional self-harm. Although no accurate description explains what leads to suicide or what comes after, it is a multifaceted phenomenon of public health urgency during a global health crisis. In the United States alone, suicide is the 10th leading cause of death and worldwide claims up to 800,000 lives each year. The international community must unite to come up with solutions to prevent the loss of life, as every single life lost is one too many.

With the COVID-19 pandemic, such an emergency naturally affects both individuals’ health and well-being and the communities in which they live. Unprecedented times unleash various emotional reactions from isolation, grief and trauma to other unhealthy behaviours, noncompliance with public health guidelines and the exacerbation of mental health conditions. While those who’ve been emotionally, sexually or physically abused in the past are more vulnerable to the psychosocial effects of a crisis, supportive interventions such as the Zero Suicide program and Cognitive Behavioural Therapy designed to promote wellness and enhance coping should be implemented [1]. 

In honour of World Suicide Prevention Week, and World Suicide Prevention Day held on the 10th of September every year, it is important to raise attention to the global importance of suicide prevention. Suicide impacts all people and particularly the world’s most marginalized and discriminated groups. It is a huge problem in developed countries and just as serious in low-and middle income countries where resources and access to healthcare professionals are scarce. In many regions of the world, the taboo and stigma surrounding suicide persist, causing people in need of help to be left alone. 

Suicide prevention with awareness campaigns ought to be prioritized on the global health and public policy agendas as a major public health issue. Routine screening for suicidal ideation by health care professionals providing care should identify and assess suicide risk among populations. According to the Diagnostic and Statistical Manual of Mental Disorders (DSM-5), risk factors of suicide include mental illness, substance use diagnoses, trauma or conflict, loss, family history of suicide, and previous suicide attempts [2].

Effectively implementing suicide prevention strategies at the populational, sub-populational and individual level requires ensuring patients’ lethal means are restricted, reduced, and that all accesss to weapons of self-harm are removed from the nearby environments. Healthcare providers should keep up to date with new developments, research, and technologies screening for suicidal ideation, allowing them to effectively serve patients beyond their clinics’ walls. Key to prevention are strong physician patient relationships that help ensure care transitions allow for physicians to act as supportive contacts reaching out with calls, texts, letters and visits to their patients particularly when services are interrupted. With access to technology the role of psychiatrists, and psychologists may continue uninterrupted as telemedicine serves as an effective platform providing patients with access to care, even during lockdowns. Besides these objectives, greater awareness and education into the community means encouraging the responsible portrayal of suicide in mainstream media. A sensitive issue of this magnitude ought to be communicated responsibly placing special attention to not trigger susceptible individuals. With school based interventions, professionals may act sooner before worsened prognosis’ effectively ensuring that access to peer support services is available. 

Suicide prevention is a responsibility of healthcare systems, medical professionals and communities. All countries must stand in solidarity and unify in collaboration to battle this common threat as preventing the tragic loss of life to suicide is of utmost importance. 

References & Further Reading

  1. In Health and Behavioral Healthcare. (n.d.). Retrieved September 14, 2020, from http://zerosuicide.edc.org/toolkit/treat/interventions-suicide-risk 
  2. Psychiatry Online: DSM Library. (n.d.). Retrieved September 15, 2020, from https://dsm.psychiatryonline.org/doi/book/10.1176/appi.books.9780890425596 
Cite this article as: Leah Sarah Peer, Canada, "Suicide – An Emergency Priority of Public Health Care," in International Emergency Medicine Education Project, October 19, 2020, https://iem-student.org/2020/10/19/suicide-an-emergency-priority-of-public-health-care/, date accessed: February 25, 2021