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: April 21, 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: April 21, 2021

Read Other Posts from Dr. Shrestha

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: April 21, 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: April 21, 2021

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

Hypokalemic Periodic Paralysis in the ED

Hypokalemic Periodic Paralysis in the ED

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:

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

Cite this article as: Sumaiya Hafiz, UAE, "Hypokalemic Periodic Paralysis in the ED," in International Emergency Medicine Education Project, September 7, 2020, https://iem-student.org/2020/09/07/hypokalemic-periodic-paralysis-in-the-ed/, date accessed: April 21, 2021

Troponin and nothing more

troponin and nothin more

It’s almost impossible to have an ER shift without encountering a chest pain patient!

The first thing that always comes to mind is to rule out STEMI; well, unless the patient is having chest pain, and you see a knife stabbed in his chest!

It’s a no brainer situation; investigations wise, you will start with an EKG, and a set of labs, including cardiac markers.

Acute coronary syndrome (ACS) with its subcategories, ST-elevation myocardial infarction (STEMI), non-ST elevation myocardial infarction (NSTEMI), and unstable angina, is responsible for one third of total mortality in individuals more than 35 years of age.(1)

The role of cardiac markers in diagnosis and management of ACS and cardiovascular problems is vital. In the United States cardiac biomarkers testing occurs in nearly 30 million emergency department visits nationwide each year.(2)

What is a biomarker?

The National Institutes of Health defined a biomarker as “a characteristic that is objectively measured and evaluated as an indicator of normal biological processes, pathogenic processes, or pharmacologic responses to a therapeutic intervention.” (3)

Biomarkers utilization in cardiovascular medicine is a wide domain; it’s used in screening, diagnosis, prognosis and monitoring. (4)

What’s available?

Numerous cardiac markers are available today and can be classified as:

  1. Biomarkers of myocardial injury, which is further divided into:
    1. Biomarkers of myocardial necrosis: CK-MB fraction, myoglobin, cardiac troponins
    2. Biomarkers of myocardial ischemia: Ischemia-modified albumin (IMA), heart-type fatty acid-binding protein (H-FABP)
  2. Biomarkers of hemodynamic stress: Natriuretic peptides (NPs): atrial natriuretic peptide (ANP), N-terminal proBNP (NT-proBNP), B-type natriuretic peptide (BNP)
  3. Inflammatory and prognostic markers: hs C-reactive protein (CRP), sCD40L, homocysteine. (4)

What’s best?

Cardiac Troponin and the B type cardiac natriuretic peptides are the two markers recommended by ACEP and AHA in diagnosis of ACS and heart failure respectively.(5)

The ACS biomarker of choice

ACS is subcategorized based on ECG and cardiac troponin. The fourth universal consensus definition of Myocardial Infarction (MI); by the European Society of Cardiology (ESC) and American College of Cardiology (ACC), takes Troponin as a detrimental parameter in case definition, because of its high sensitivity and specificity.(6)

ACEP and AHA guidelines recommend the use of Troponin as level A class 1 in diagnosis of ACS. (7) It was practiced before to consider multiple markers dealing with ACS, more precisely in NSTEMI ruling out recommendation. However, this practice is now outdated with the use of hs cT solely.(7-9)

What’s troponin and why do we like it?

It’s a protein that regulates the interaction between actin and myosin filaments, found in skeletal and cardiac myocytes. Cardiac troponin (cTn) has three subunits troponin T, troponin C and troponin I. Troponin T and I are highly specific and sensitive.(10) The half-life of troponin T and troponin I in the blood is about 2 hours and last in serum for 4 to 10 days10

For ACS, the sensitivity of troponin is about 95%, and the specificity is about 80%, higher than any other marker available.(12)

However, many causes can elevate serum troponin which includes pericarditis, myocarditis, heart failure and chest trauma; non-cardiac conditions are sepsis, renal disease, pulmonary embolism, COPD, strenuous exercise and hypertension.(14)

High-sensitivity cardiac troponin (hs-cTn T and I) can detect troponin at concentrations much lower than the old cTn tests, and has replaced it.7 For ACS, hs cT substituted and limited the roles of other markers; it’s proven to be safe, cost effective, and a valuable prognostic factor. (7-9, 14)

For all of the above and the heart score… In ACS, use Troponin and nothing more!

References and Further Reading

  1. Anumeha Singh; Abdulrahman S. Museedi; Shamai A. Grossman. Acute Coronary Syndrome. StatPearls[Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan.
  2. Alvin MD, Jaffe AS, Ziegelstein RC, Trost JC. Eliminating Creatine Kinase–Myocardial Band Testing in Suspected Acute Coronary Syndrome: A Value-Based Quality Improvement. JAMA Intern Med. 2017;177(10):1508-1512. doi:10.1001/jamainternmed.2017.3597.
  3. Biomarkers and surrogate endpoints: preferred definitions and conceptual framework. Biomarkers Definitions Working Group. Clin Pharmacol Ther. 2001 Mar; 69(3):89-95. doi.org/10.1067/mcp.2001.113989.
  4. Jacob R, Khan M. Cardiac Biomarkers: What Is and What Can Be. Indian J Cardiovasc Dis Women WINCARS. 2018 Dec; 3(4): 240–244. doi: 10.1055/s-0039-1679104.
  5. Richards AM. Future biomarkers in cardiology: My favourites. European Heart Journal Supplements, Volume 20, Issue suppl_ G, 1 August 2018, Pages G37-G44. doi.org/10.1093/eurheartj/suy023.
  6. Thygesen K, Alpert JS, Jaffe AS, et al., on behalf of the Joint European Society of Cardiology (ESC)/American College of Cardiology (ACC)/American Heart Association (AHA)/World Heart Federation (WHF) Task Force for the Universal Definition of Myocardial Infarction. Fourth Universal Definition of Myocardial Infarction (2018). J Am Coll Cardiol. 2018. Volume 72 DOI: 10.1016/j.jacc.2018.08.1038. 
  7. Ezra A. Amsterdam, Nanette K Wenger, Ralph G. Brindis, Donald E. CaseyJr, Theodore G. Ganiats, David. HolmesJr, Allan S. Jaffe, Hani Jneid, Rosemary F. Kelly, Michael C. Kontos, Glenn N. Levine, Philip R. Liebson,Debabrata Mukherjee, Eric D. Peterson, Marc S. Sabatine, Richard W. Smalling, Susan J. Zieman. 2014 AHA/ACC Guideline for the Management of Patients With Non–ST-Elevation Acute Coronary Syndromes: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation. 2014; 130:e344–e426. 2014. doi.org/10.1161/CIR.0000000000000134.
  8. Edward W Carlton, Louise Cullen, Martin Than, James Gamble, Ahmed Khattab, Kim Greaves. A novel diagnostic protocol to identify patients suitable for discharge after a single high-sensitivity troponin. Heart. 2015 Jul 1; 101(13): 1041–1046. doi: 10.1136/heartjnl-2014-307288.
  9. Ron M. Walls, Robert S. Hockberger, Marianne Gausche-Hill, Katherine Bakes, Jill Marjorie Baren, Timothy B. Erickson, Andy S. Jagoda, Amy H. Kaji, Michael VanRooyen, Richard D. Zane. Rosen’s Emergency Medicine: Concepts and clinical practice. 9th edition. Elseivier; 2018.
  10. Ooi DS1, Isotalo PA, Veinot JP. Correlation of antemortem serum creatine kinase, creatine kinase-MB, troponin I, and troponin T with cardiac pathology. Clin Chem. 2000 Mar; 46(3):338-44.
  11. Harvey D. White, DSC. Pathobiology of Troponin Elevations: Do Elevations Occur With Myocardial Ischemia as Well as Necrosis?. Journal of the American College of Cardiology. Vol. 57, No. 24, ISSN 0735-1097/$36.00 Published by Elsevier Inc. doi:10.1016/j.jacc.2011.01.029.
  12. John E. Brush, Jr., Harlan M. Krumholz. A Brief Review of Troponin Testing for Clinicians. American College of Cardiology. 2017 Aug 7th. acc.org/latest-in-cardiology/articles/2017/08/07/07/46/a-brief-review-of-troponin-testing-for-clinicians.
  13. Asli Tanindi, Mustafa Cemri. Troponin elevation in conditions other than acute coronary syndromes. Vasc Health Risk Manag. 2011; 7: 597–603. PMID: 22102783. doi: 10.2147/VHRM.S24509.
  14. Donald Schreiber, Barry E Brenner. Cardiac Markers. emedicine.medscape.com/article/811905-overview [Accessed 2020 March 23rd].
Cite this article as: Israa M Salih, UAE, "Troponin and nothing more," in International Emergency Medicine Education Project, August 19, 2020, https://iem-student.org/2020/08/19/troponin/, date accessed: April 21, 2021

Better Decisions

Better Decisions

Why is a physician working in the Achham district of Nepal worried when he finds that a patient tested positive for HIV, but a physician working in Humla district is worried but also skeptical? Why do we generally not prescribe high dose IV Vitamin C + Thiamine + Hydrocortisone when the combination has shown to provide a substantial mortality benefit in sepsis? Why do we encourage a patient, very rightly so, to get flu shots every year?

When making decisions, we think, we use our knowledge, weigh pros and cons, and make a choice. The variables, whose salient feature is that we barely think of them, are biases and heuristics. We are influenced by various medical journals we read, colleagues we work with, and even movies and advertisements we watch. Another, sometimes lethal feature of these decision influencers is that their influence is inversely proportional to the time we have to make a choice. This becomes relevant in ED, where split-second decisions are the norm.

So how do we make decisions that are backed more by studies and less by our implicit biases? How do we compare two tests that measure the same variable or two vaccines that work against the same infectious agent? There comes the role of statistics. Every physician, especially those making life-saving decisions in a fraction of seconds, should have an intuitive understanding of medical statistics. This will help us make decisions that are backed by our best understanding and understand our limitations.

Achham district of Nepal has the highest prevalence of HIV/AIDS in the country. When the disease’s prevalence is high, the chance that your patient has the disease given the positive result is high. This is the Positive Predictive Value (PPV). The same physician would want to re-run the test on asymptomatic patients if the test was negative. That is because, given the high prevalence, the Negative Predictive Value (NPV) of the test is low. One would also worry about the sensitivity and specificity of the test in question. Although these are properties intrinsic to the test and do not change with the prevalence of a disease in a population, their knowledge adds to the confidence with which we can prescribe a test to a patient.

One way of thinking about sensitivity is: among 100 diseased patients, how many will the test identify? You would want your screening test to have very high sensitivity so that you do not miss any diseased person. Specificity can be thought of as: among 100 healthy patients, how many will the test identify as negative for the disease? If a highly specific test tells you that a patient has a disease, chances are – he does. So the worried physician of Achham district probably used a very sensitive test and followed it with a highly specific test to confirm before talking to the patient about the result.

We encourage all patients to get the flu vaccine every year because of something called the Number Needed to Treat (NNT). It is the number of patients you need to treat to prevent one additional bad outcome e.g., severe flu, death, etc. Every 12 – 37 flu shots prevent one healthy adult from influenza when the vaccine is well-matched. That means the NNT of the flu vaccine is 12 to 37. [1]

The combination of high dose IV vitamin C + Thiamine + Hydrocortisone had shown to provide a substantial mortality benefit in a small retrospective study in 2016. We generally do not prescribe this in sepsis because we do not have a large RCT that supports the claim yet. The GRADE working group suggests a system for grading the quality of evidence. [2] When we say that evidence is graded 1A or 3B, we are commenting on the type, quality, and the number of studies that back the claim. Familiarizing ourselves with the grading system and hierarchy of evidence can be a good start in the world of evidence-based medicine.

References

  1. Kolber MR, Lau D, Eurich D, Korownyk C. Effectiveness of the trivalent influenza vaccine. Can Fam Physician. 2014;60(1):50.
  2. Petrisor B, Bhandari M. The hierarchy of evidence: Levels and grades of recommendation. Indian J Orthop. 2007;41(1):11-15. doi:10.4103/0019-5413.30519
Cite this article as: Sajan Acharya, Nepal, "Better Decisions," in International Emergency Medicine Education Project, July 27, 2020, https://iem-student.org/2020/07/27/better-decisions/, date accessed: April 21, 2021

Knee Jerk, Shotgun and Kitchen Sink in Emergency Medicine

Knee Jerk, Shotgun and Kitchen Sink in Emergency Medicine

For a trainee in EM, it is useful to know about three types of cognitive practice that require caution.

While a knee jerk reaction may sometimes save time, a shotgun investigation may improve billing and a kitchen sink therapy may create the illusion of therapeutic rigor, arguably that’s all there is to it.

In reality, there is not much true value to any of these three missed approaches.

We will look at each one with a few examples and then briefly discuss below.

Knee Jerk

When I was rotating in the ED as an MS4, a visiting EM attending once told me that “adding a Type and Rh should become a knee jerk” for any patient with vaginal bleeding in early pregnancy. Whether or not taking the extra 30 seconds to scroll through the EMR for a previously documented Rh likely to be on file is a better strategy, this one is fairly simple.

Not all of our knee jerk reactions are equally simple or harmless.

I have seen adenosine being pushed before one could say “Mama” for anything from sinus tach to atrial flutter and A-fib with RVR: paramedics, physicians and even unsupervised nurses all being equally guilty. Why? Because a sustained heart rate above 180 is scary to some. And the reflex is to do something quickly because we don’t like to remain scared.

Nursing staff going straight for IV placement while forgetting not only the basic ABCs of resuscitation but even to disrobe the patient is another example. Starting any patient at 100% oxygen saturation who is short of breath on nasal cannula oxygen is yet another.

We like to do what we are trained to do well and/or what is easy. Our brains then compel us to prioritize doing it.

Once my ED team halted a verbal order for a whopping dose of colchicine blurted out to nursing by a careless consulting cardiology fellow – the patient had mentioned his ankle pain to the fellow in passing. The man was in acute renal failure and ended up with a septic ankle joint diagnosed later. Knee jerk is in part responsible for well-perpetuated ED mental formulas such as “gout = colchicine”, “fever = paracetamol”, “wheezing = albuterol” and “hypotension = 2 liter IV fluid bolus”.

The knee jerk is how we pick from our favorite antibiotics and how we generally prescribe, how we diagnose and order things on lobby and triage patients and how we even decide on CT scans and dispositions. Frequently, our hospitalist medicine colleagues will utilize the same reflex and unnecessarily or prematurely consult specialists.

On occasion, when the arrow released via a knee jerk reaction hits the bull’s eye, it feels and looks great. Knee jerk, unfortunately, is also how we assume, stereotype, over-simplify, ignore and ultimately miss.

Shotgun

This one does not have to be shot from the hip, though it certainly looks cooler that way. Often this is done thoughtfully, with a pseudo-scientific aroma to it.

I was on my MS3 internal medicine rotation when one day, the dreaded ED handed us an elderly female with a congratulatory thick paper chart, a bouquet of vague complaints and no clear diagnosis. When I asked my senior resident what we should do, the answer was a shoulder shrug and a confident “Lab ‘er up!”.

Shotgunning is not just about shooting out labs in the dark, however. It usually refers to a much wider “strategy” (actually, a lack thereof) of checking anyone for “anything” so as to not miss “something”.

Consider an ED evaluation of a headache involving some component of facial pain. Let’s order a migraine cocktail, CT and CTA of the head and neck, ESR to check for temporal arteritis; and when we find nothing, let’s do antibiotics in case of possible dental caries, otitis, mastoiditis or sinusitis. Sounds pretty thorough and terrific, doesn’t it? In fact, many patients would tend to think so. Clearly, after all that, we just could not miss something real badTM. We should remember that in EM you are worth every test that you order.

Hyperlaboratoremia and panscanosis are not the only clinical manifestations of the shotgun approach.

Though in all places, it is well-intended, there is a more buried shotgun in standardized chest pain workups, ED triage scales, pre-conceived clinical pathways and universal screenings than you may think.

Kitchen Sink

One might say that kitchen sink is the therapeutic twin of shotgun diagnostics, though one does not need to stem from the other.

The kitchen sink is how you and I treat most non-threatening and hence not easily identifiable ED rashes. As one of my professors once said: the rule of dermatology is that “if it is dry, use a wetting agent, if it is wet, use a drying agent, plus steroids and antibiotics for everyone”.

At its core, any kitchen sink approach violates two key pillars of modern medicine – evidence-based practice and personalized therapy.

Another example is the kitchen sink phase of resuscitation in a soon to be aborted CPR effort. While in the beginning, we do tend to follow certain parameters and algorithms, towards the end and well into the “futile” stage of CPR remedies like calcium, magnesium, bicarbonate, second and third anti-arrhythmic and so on all inevitably flow one after another regardless of the suspected cause of cardiac arrest or objective facts known.

While benign rashes are benign, and futile CPR is futile, most of the kitchen sink does not involve such obvious extremes. In fact, some of it is perfectly legitimized and even justified – have you ever thought of what “broad-spectrum antibiotics” in sepsis really implies?

Reasons For Need To Know

Why is knowing about the knee jerk, the shotgun and the kitchen sink ahead of time important?

First, the cognitive action patterns described are unavoidable and inescapable. It is precise because we will not be able to fully stop using all three on occasion, that we should know about them ahead of time.

Second, there is something positive and well-thought-out corresponding to the other side of each of the three behaviors:

Fundamentally, knee-jerk reactions rest on pattern recognition as the predominant cognitive pathway at work – something that physicians start to rely upon more and more as they mature. While risking the error of premature diagnostic closure (among others), pattern recognition does save time and resources. This mode is why, as some studies suggest, senior-most providers may be more effective in triage.

On the opposing side of the shotgun coin are the well-accepted mantras of keeping one’s differentials broad and of thinking outside the box. Such forced mental efforts help avoid anchoring among other cognitive errors.

Last, kitchen sink elements may indeed be acceptable in salvage type of situations or in uncharted waters, given multiple paucities in our scientific evidence and in our full understanding of physiologic processes. In such select cases, we humbly admit our limits and hope that something unknown may work at the last minute, while there is no further harm that can be done.

It would be a mistake, however, to confuse each of the positives described with the three patterns we started with when taken in their pure form.

Third, the limitations and harms encountered by not keeping the three tendencies in check are real and immediate:

  • Knee-jerk reactions do not yield beneficial results when the situation encountered is new and principally different from those experienced before, yet it has the external appearance of something familiar. Think of COVID.
  • Shotgun-galore practices subject multiple patients to unnecessary tests and to potentially harmful procedures and interventions that inevitably follow, further inflating the costs of healthcare.
  • Perpetuating myths and unmerited traditional practices, kitchen sink therapies also coach our patients into expecting both the unreasonable and the unnecessary for the next visit, undermining any accepted standard of care at its very core.

What Next?

A more in-depth discussion of all three phenomena presented would indeed be appropriate, including an investigation into any viable alternatives.

For now, I encourage all trainees to look further into the general and well-researched topic of cognitive errors in emergency medicine. 

We should also all strive to practice based on best available evidence and not to be coerced into questionable behaviors by external pressures such as performance metrics that may lurk as false substitutes for quality.

References and Further Reading

  • Frye KL, Adewale A, Martinez Martinez CJ, Mora Montero C. Cognitive Errors and Risks Associated with Provider Handoffs. Cureus. 2018;10(10):e3442. Published 2018 Oct 12. doi:10.7759/cureus.3442
  • Oliver G, Oliver G, Body R. BET 2: Poor evidence on whether teaching cognitive debiasing, or cognitive forcing strategies, lead to a reduction in errors attributable to cognition in emergency medicine students or doctors. Emerg Med J. 2017;34(8):553-554. doi:10.1136/emermed-2017-206976.2
  • Schnapp BH, Sun JE, Kim JL, Strayer RJ, Shah KH. Cognitive error in an academic emergency department. Diagnosis (Berl). 2018;5(3):135-142. doi:10.1515/dx-2018-0011
Cite this article as: Anthony Rodigin, USA, "Knee Jerk, Shotgun and Kitchen Sink in Emergency Medicine," in International Emergency Medicine Education Project, July 20, 2020, https://iem-student.org/2020/07/20/knee-jerk-shotgun-and-kitchen-sink-in-emergency-medicine/, date accessed: April 21, 2021

A simple cellulitis of the foot?

a simple cellulitis of the foot?

Case Introduction

A 47 year old woman comes to a community ED complaining of pain and redness in her right foot developing quickly over two days. She denies any trauma and otherwise feels well. She is not sure, but may have had a “sore” near her toes that has already healed. Patient has diabetes but is normoglycemic. She has no prior history of cellulitis, joint infections or gout. There is no history of immunocompromise, including steroids, or any IV drug use. All vitals are within normal limits and review of systems is negative for fever, chills, respiratory or gastrointestinal symptoms.

On exam, there is generalized edema, erythema and tenderness, but no tenderness out of proportion, and no open sores or ulcerations. A sub-acute appearing callus is apparent on the plantar surface opposite fifth and fourth distal metatarsals. The ankle joint is tender but less so than the foot, and ranging it does not elicit more pain than at baseline. Distal sensation, pulses and toe motion are intact, though capillary refill is slightly delayed.

cellulitis - foot
cellulitis - foot 2

Initial Questions

Basic labs obtained are unremarkable and patient is receiving IV broad spectrum antibiotics, including MRSA coverage. Plain films are obtained, and there is some concern for small air pockets in the soft tissues.

cellulitis - xray 2
cellulitis - xray

A phone consultation with podiatry is obtained. A decision is made to take the patient to the OR on the same evening. No further imaging or diagnostic studies are advised.

Additional Questions

After the callus is taken off in the OR, large amount of frank pus is obtained that tracks all the way to the third metatarsal. A debridement is performed, and long term antibiotics with close follow up are needed. Overall impression was that while no necrotizing infection was found, any further delay would have risked a trans-metatarsal amputation (at the least).

Key Points

While we do not have room for a lengthy discussion on differentiating plain cellulitis from “other”, it is worthwhile to note several things:

Cite this article as: Anthony Rodigin, USA, "A simple cellulitis of the foot?," in International Emergency Medicine Education Project, February 7, 2020, https://iem-student.org/2020/02/07/educational-case-a-simple-cellulitis-of-the-foot/, date accessed: April 21, 2021

Further Reading

Sickle Cell, Pain and the Emergency Department

Sickle Cell Disease

It’s 2 AM, and the Pediatric Emergency Department (ED) at a community  hospital in New York is overflowing with children and caregivers. A young Nigerian boy is being transported down the center of a hallway, past a long line of doors to patient rooms. The porter is calm and walks briskly, determined to bring this boy to get immediate care. The boy winces, his hands outstretched next to him, rigid, and frozen in space, and while he is seated in the wheelchair, his legs bent at the knees are thin frames, held in place with his feet planted on the wheelchair pedestals. He is afraid to move any of his extremities; tears are rolling down his face; he is fighting the urge to grimace and furrow his brow. He cries how much it hurts to move. He knows he needs help.  Behind him, his mother follows close holding a one-year-old baby in her arms, and behind her, five other young children aged 3 through to thirteen stream in. There is quiet concern on all of their faces. The older siblings have seen this before. We learn that he has Sickle Cell Disease (SCD). He has been in excruciating pain for the past 4 hours and is now presenting with dactylitis. This case has not been the first in this ED, and like other EDs across the United States and in the world, the number of cases presenting with SCD will increase.

Sickle Cell Disease in the Emergency Dept: a global public health issue iEM Dhir

Sickle Cell Disease (SCD)

SCD is a condition that causes red blood cells to morph from a biconcave dumbbell-shaped disc, into a rigid semi-circular shape. This disease is inherited genetically by receiving two sickle genes, one from each parent and risk for complications are attributed to a variety of factors, including deoxygenation, dehydration. It is most common in African Americans as well as Latinos and people of Middle Eastern, Indian, Asian and Mediterranean backgrounds.  In the United States, SCD is the most common genetic blood disorder and affects approximately 100,000 Americans(1) and although babies are screened at birth, management plans vary with the degree of disease progression and exacerbation severity, as well as with the availability of resources and education.

RBCs in Sickle Cell Disease
Image: Sickle cells and normal red blood cells from Sickle Cell Disease, Genome. Gov

Why Emergency Physicians need to be Familiar with SCD

SCD affects both pediatric and adult patients, and it has been reported that patients between the ages of 18 to 30 years old have increased emergency department utilization. A major reason for this is due to the transition by young adults from pediatric to adult care in the management of SCD, and this population is simultaneously also learning to navigate the health care system and community resources (pediatric to adult care, insurance, independent decision making, housing, education, workforce) as discussed further below(2). In addition, the use of community health workers is important as they can act as liaisons between the health care systems and patients to disseminate information and resources. However, despite the awareness of the disproportionate use of the ED among patients with SCD, the social factors that impact care remain unknown(3) and more research and investigation is needed to understand this patient population.

Often when a complication or crisis occurs in patients with SCD, patients seek immediate care in the Emergency Department. Included in the potential list of complications include infections, such as those with encapsulated bacteria; sepsis; stroke; splenic sequestration, and early treatment is essential in managing patients. Of these complaints, the emergent cases to be aware of in the ED include vaso-occlusive crisis and pain, sickle cell anemia (SCA)(4) central nervous system such as stroke, and acute chest syndrome (ACS), where ACS due to blocked capillaries in the lungs, may be caused by infections, asthma exacerbations and/or pulmonary embolisms, and is the leading cause of morbidity in patients with SCD. Further, the Emergency Severity Index (ESI) Version 4 triage system, commonly used in the majority of EDs in the United States, suggest that patients with SCD be triaged as ESI level 2, indicating a very high priority, and that rapid placement be facilitated(5).

Although the discussion of complications of SCD including the presentation and management is a complex topic, and will be covered in detail in future posts, information and algorithms for clinicians are available online for reference. One such resource is a treatment algorithm that acts as a how-to guide for SCD and is available online in the Annals of Emergency Medicine(6). This approach is based on the point-of-care hemoglobin level, and discusses issues such as myonecrosis, aplastic crisis, ACS.

Sickle Cell Disease in the Emergency Dept: 1 in 4 patients in the USA with SCD receive standard care iEM Dhir

Pain in SCD

When tissues and organs are not adequately perfused with oxygen, in part due to the sickled shape of RBCs, tissue damage and death can occur. Patient management of vaso-occulusive crisis and pain varies by practices and the medications available for use around the world, however it is important to note that pain in patients with SCD is often extreme and may require treatment with opioids. In a response to the American Society of Hematology (ASH) draft recommendations to Sickle Cell Disease-Related Pain in May 2019(7),  emDOCs.net published a response to the drafted recommendations and offered insight to pain management and includes an algorithm(8). The insight provided is essential in decreasing the suffering experienced by patients during an SCD crisis, and notes the use of Dilaudid, Ketamine, Dexmedetomidine, and Lidocaine. Further, the understanding of limiting the use of NSAIDS due to impaired renal function caused by the disease is also outlined in the response.

Management of pain in pediatric patients with SCA and vaso-occulsive pain also varies according to hospital and individual provider practices, and scientific investigation and patient research is needed to provide proper care to this population. An example includes a study by PECARN addressing the use of a normal saline bolus in pediatric emergency departments found an association with poorer pain control(9). Identifying and implementing results from research studies is important in understanding and managing SCD in both adult and pediatric patients.

Emergency Physicians around the world should be aware of strategies for identifying SCD, and management, specifically in areas around the world where refugees from countries with SCD prevalence is common. Countries where refugees and migrants are commonly are known to disembark, such as those in southern Europe(10) and certain areas in the United States and Canada would benefit from in-depth analysis of the issue and could allow for appropriate and accessible health care to vulnerable populations, as well as educate providers who are unexposed to managing emergencies in SCD patients while setting in place integrated and individual health plans away from emergency room dependence(11). In developing countries with SCD populations, such as Nigeria, there is a high prevalence of pediatric emergency cases, and the proper management of the disease as well as policy and hospital organization for high volume and off-hour admissions, may reduce hospital stays(12). Further, the self-efficacy of adult patients with SCD, from education, pro-active efforts, understanding of disease management, also can allow for decreased ED visits and hospitalizations for pain(13).

SCD affects approx 100,000 Americans Sickle Cell Disease in the Emergency Dept iEM Dhir

Investigations, Resources, Education

A number of investigative studies, clinical trials and research is being conducted around the world for a better understanding of SCD, including patient care in adult and pediatric patients, genetic factors, supportive services, associated co-morbidities, and search for cures. Investigations around the world include collaborations and information sharing between academic researchers, patients, clinical providers, and health care providers and officials around the world.

The National Heart, Lung, and Blood Institute hosted a series of Webinars in September 2018, during Sickle Cell awareness month from experts in blood science and sickle science research and are available to watch for free online(14). Some of the key highlights from two of the webinars: Serving the Sickle Cell Disease Community Here and Abroad; Sickle Cell Transitional Care from Childhood to Adulthood, are discussed here.

SCD occurs in 1 out of ever 365 Black or African American births, Sickle Cell Disease in the Emergency Dept, iEM Dhir

Webinar Overview Serving the Sickle Cell Disease Community Here and Abroad
Presented by Dr. Keith Hoots, Director of Division of Blood Diseases and Resources, NHLBI
  • Prevalence of the disease is so much larger in Africa than most places in the world. There are as many babies born with SCD born in Nigeria there are babies born with SCD, by estimate, as there almost are total people with SCD in the United States.
  • There is a need to share research and practices in the developed world with the developing world.
Three New Research Initiatives in Africa:
  • The Sickle Pan-African Research Consortium (SPARCO)
    Overview: The study sites for this research include East Africa (Tanzania), West Africa (Ghana, Nigeria) and central Africa (Cameroon, Democratic Republic of Congo) with the goal to later include 20 sites in 15 countries. SPARCO’s aim is to develop an SCD database, standards of care, and strengthen research investigation.
  • Realizing Effectiveness Across Continents With Hydroxyurea (REACH):
    Overview: Safety and dosing of hydroxyurea therapy for SCA in pediatric patients in sub-Saharan Africa; sponsored by the Children’s Hospital Medical Center, Cincinnati
  • Sickle Cell Disease Genomics of Africa (SickleGenAfrica)
    Overview: The purpose is to develop strategies to predict, prevent and treat organ damage in SCD and to investigate biomarkers associated with the development of organ damage, including molecules released during red blood cell damage in sub-Saharan African populations.
Webinar Overview: Sickle Cell Transitional Care from Childhood to Adulthood
Part 1 Presented by Dr. David Wong, MD, FAAP, Medical Officer, Office of Minority Health
  • SCD is no longer a childhood disease. Young adults are at a higher risk for hospitalization due to illness and pain.
  • Treatment and management examples in childhood include annual transcranial dopplers to assess for risk of stroke; vaccinations; hydroxyurea; L-glutamine; opioids for pain management; penicillin prophylaxis; RBC transfusions;  water intake to avoid exacerbations due to dehydration; splenectomy. The cure available is bone marrow transplant.
  • Prior to July 2017, Hydroxyurea was the only FDA approved therapy for 20 It is used in adults and children. It has been shown to reduces hospital admissions, pain crisis, and ACS however barriers to hydroxyurea use exist. These include difficulty with communicating the use to patients and caregivers, issues with frequent monitoring, lack of adherence, lack of provider knowledge and comfort with its use.
  • Community Health Workers (CHWs) are key players in effective patient care. CHW can provide information affected by social and health determinants from local economic and environmental (housing, employment), local communities (families, safety, support), activities (learn, work, play, move, shop), lifestyles (alcohol, drugs, smoking, sexual health, physical activity, and individual needs (age, genetics). CHW are experts in condition-specific information and navigating complex health systems, including accessing care in a medical home (the approach to providing comprehensive care). This is particularly important when care is not always contained or organized by one organization, where care should be accessible, continuous, comprehensive, family-oriented, coordinated, compassionate and culturally competent. Pediatric medical home principles include family-centered partnerships, community-based systems, transition care, value.  Interventions for education such as warning signs and treatment options and links to care are important.
  • The SCD Newborn screening program, and the Sickle Cell Disease Treatment Demonstration Program for patients who solely rely on the ED for SCD care, aid the care options for patients with SCD.

Follow this iEM story for part two which will include information on adult and pediatric management of SCD in the ED, as well as an overview of four NHLBI webinars: Holistic Health and Sickle Cell Disease A Focus on Mental and Behavioral Health; Genetic Therapies in Sickle Cell Disease; Bone Marrow Transplants, Other Therapies, and Sickle Cell; Improvement Initiatives and Ongoing Research.

SCD occurs 1 out of ever 16,300 Hispanic-American birthds, Sickle Cell Disease in the Emergency Dept, iEM Dhir

Further Reading

Emergency Department Sickle Cell Care Coalition: Resources
https://www.acep.org/by-medical-focus/hematology/sickle-cell/resources/

National Institute of Health’s Cure Sickle Cell Initiative:
https://www.nhlbi.nih.gov/science/cure-sickle-cell-initiative

2019 sickle cell disease guidelines by the American Society of Hematology: methodology, challenges, and innovations: https://www.ncbi.nlm.nih.gov/pubmed/31794603

Sickle Cell Disease Training And Mentoring Program (STAMP): https://www.minorityhealth.hhs.gov/sicklecell/#stamp

Episode 68 Emergency Management of Sickle Cell Disease: https://emergencymedicinecases.com/emergency-management-of-sickle-cell-disease/

Practice Variation in Emergency Department Management of Children With Sickle Cell Disease Who Present With Fever. https://www.ncbi.nlm.nih.gov/pubmed/30020250

 

References

1 Centers for Disease Control and Prevention: Sickle Cell Disease 

2 Sickle Cell Transitional Care from Childhood to Adulthood: Youtube

3 Journal of Pediatric Hematology/Oncology. 42(1):e42–e45, JANUARY 2020, DOI: 10.1097/MPH.0000000000001669 PMID: 31743315

4 Porter M. Rapid fire: sickle cell disease. Emerg Med Clin North Am. 2018;36:567–576

5 Evidence Based Management of Sickle Cell Disease: Report

6 Sickle Cell Crisis and You: A How-to Guide, Raam R., Mallemat H., Jhun P., Herbert M. (2016)  Annals of Emergency Medicine,  67  (6) , pp. 787-790

7 The American Society of Hematology Website: 

8 ED Management of Sickle Cell Vaso-occlusive Crises: Myths, Facts, and A Novel Approach to Acute Pain Management, EMdocs.net website

9 Normal saline bolus use in pediatric emergency departments is associated with poorer pain control in children with sickle cell anemia and vaso-occlusive pain, Am J Hematol. 2019 Jun;94(6):689-696

10 Lucia De Franceschi, Caterina Lux, Frédéric B. Piel, Barbara Gianesin, Federico Bonetti, Maddalena Casale, Giovanna Graziadei, Roberto Lisi, Valeria Pinto, Maria Caterina Putti, Paolo Rigano, Rossellina Rosso, Giovanna Russo, Vincenzo Spadola, Claudio Pulvirenti, Monica Rizzi, Filippo Mazzi, Giovanbattista Ruffo, Gian Luca Forni; Access to emergency departments for acute events and identification of sickle cell disease in refugees. Blood 2019; 133 (19): 2100–2103

11 Sickle Cell Disease Training And Mentoring Program Website 

12 Robert M Cronin, Tim Lucas Dorner, Amol Utrankar, Whitney Allen, Mark Rodeghier, Adetola A Kassim, Gretchen Purcell Jackson, Michael R DeBaun, Increased Patient Activation Is Associated with Fewer Emergency Room Visits and Hospitalizations for Pain in Adults with Sickle Cell Disease, Pain Medicine, Volume 20, Issue 8, August 2019, Pages 1464–1471

13 Enyuma, Callistus Oa et al. “Patterns of paediatric emergency admissions and predictors of prolonged hospital stay at the children emergency room, University of Calabar Teaching Hospital, Calabar, Nigeria.” African health sciences vol. 19,2 (2019): 1910-1923. doi:10.4314/ahs.v19i2.14

14 National Heart, Lung, and Blood Institute Webinars

* Images from The Sickle Cell Disease Tool Kit.

Cite this article as: Bryn Dhir, USA, "Sickle Cell, Pain and the Emergency Department," in International Emergency Medicine Education Project, January 27, 2020, https://iem-student.org/2020/01/27/sickle-cell-pain-and-the-emergency-department/, date accessed: April 21, 2021

Clinical examination of the hemodynamically unstable patient

Clinical examination of the hemodynamically unstable patient

Authors: Job Rodríguez Guillén. Chief of Emergency Department. Hospital H+ Querétaro. México and Paola Rivero Castañeda. Medical Intern, Anahuac Querétaro University, Mexico. 

Introduction

Clinical examination accounts as a fundamental part in the management of most critical scenarios. Although there are few publications and it remains controversial, its value considered as limited by 50% of medical practicioners (1). None of the well-known semiology books include any section about the physical examination in the critically ill patient (2). Nonetheless, an adequate clinical evaluation at the patient’s bedside may save lives in the context of a serious situation.

Clinical Examination Objectives

The main objectives are identifying and discerning from types of shock, emphasizing in the identification of life-threatening conditions, clinical signs of organic hypoperfusion, as well as to evaluate treatment response regarding therapies employed, and risk stratifying.

Identify hemodynamic instability

  • Life-threatening conditions (Tension pneumothorax, Cardiac tamponade, Pulmonary thromboembolism, Active hemorrhage, etc.)
  • Organ hypoperfusion
    (Altered mental state, decreased uresis, mottled skin, prolonged CFT, etc.)

Evaluate treatment response

  • Vital signs and normalization of the clinical state
    (Mental state improvement, diminished skin mottling, improved uresis, normalization of prolonged capillary filling time, etc.)

Risk stratifying

  • Scale and prognostic scores calculation. Prognostic scores use a combination of clinical and/or laboratoy variables (SOFA: Squential Organ Failure Assessment; APACHE: Acute Physiology and Chronic Health Evaluation; SAPS: Simplified Acute Physiology Score; MPM: Mortality Probability Models, etc.)

Clinical Exam Systematization

The clinician must be able to do a quick and efficient clinical examination to recognize different states of shock as early as possible, or even situations that may compromise organic perfusion. At a given time, it’s suggested to check out the clinical history, re-interrogate the patient and his/her family members, as well as patient’s family/regular physician (or even look for their previous medical notes), in order to help clinical integration, and so for decision making.

Systematization of the evaluating process, based on the previously proposed objectives, can be identified with the following mnemonic: PROA.

PROA - Summary

P - Probabilistic thinking

  • Think about any probability.
  • Look for intentionally.
  • Analyze clinical context and individualize.

R - Risk of dying

Identify life-threatening causes: Cardiac tamponade, Tensionpneumothorax, Pulmonary thromboembolism, Active hemorrhage, etc.

O - Organic hypoperfusion

Cutaneous perfusion signs: examine mottled skin and capillary filling time.

A - Approach of the clinical examination

Clinical exam by regions. Some components may not be relevant for all patients, even requiring other physical maneuvers. Even though laboratory and imaging are not part of the clinical exam, their interpretation must be integrated with the examination findings.

Probabilistic Thinking

Medicine is a science of uncertainty and an art of probability.

— William Osler

Clinical decision making in the emergency department begins with the estimation of the probability of a determined patient to have or do not have specific conditions (Bayesian reasoning or pretest probability).

Example; the probability of septic shock in a young patient after having a car crash is very low compared to the high probability of presenting with hemorrhagic or obstructive shock.

Proposed decisions related to initial probabilistic thinking vary in clinical relevance depending on the patient’s condition. It should always be re-evaluated through available additional data (posttest probability) (Figure 1).

Relationship between probability thresholds and decision‐making zones
Figure 1: Relationship between probability thresholds and decision‐making zones (3).

Risk of Dying

Shock is a momentary pause in the act of death.

— John Collins Warren

Currently, there are four types of shock, all with a common pathophysiological pathway: acute circulatory insufficiency associated with cell oxygen utilization dysfunction (altered-balance between oxygen input and consumption: DO2/VO2 dysfunction), a central situation that takes part in the development of multiorgan dysfunction (4-5).

Initial physical examination should be directed to the identification of immediate life-threating pathologies such as obstructive shock (Tension pneumothorax, cardiac tamponade, pulmonary thromboembolism), hemorrhagic shock etc.

These pathologies require immediate action. Otherwise, early multi-organ dysfunction and death may occur. The Point of Care Ultrasound (PoCUS), is a fundamental tool used for the evaluation of patients with hemodynamic instability of unknown origin.

Organ Hypoperfusion

When assessing the damage an earthquake or fire has caused inside a building, one looks through the windows. Using this analogy, it would be useful to be able to see inside the body to view the damage caused by the shock process.

— Jean-Louis Vincent

The initial approach to clinical examination begins with the skin. It is essential to remember that microcirculation cannot be globally defined through its dependency with macrocirculation, autoregulation mechanisms and organ interactions. Moreover, the availability of devices to evaluate it remains limited. Therefore, the evaluation is done from clinical, biochemical and hemodynamic data integration (6) (Figure 2)

Figure 2: three windows of shock

The correct way of measuring capillary filling time

Approach of The Clinical Examination

Clinical exam is not an art, is an essential ability.

— Leonel Martínez-Ramírez

During the initial evaluation, multiple situations can affect the accomplishment of a detailed physical examination. Therefore, it is recommended to follow a structured exploration method, looking at every main organ system and region. Documenting its results would allow avoiding the inclusion of essential data, and would permit to identify tendencies or any change in the patient’s clinical status.

Clinical examination approach in the critically-ill patient.

7Clinical examination approach emphasized in the critically-ill patient. This examination is realized based on every region in the body. Some components may not be relevant for all patients, or even some other maneuvers shall be executed in the physical examination. The verification list should be modified to be adapted to each patient’s circumstances. Laboratory and other studies analysis does not conform part of the clinical examination, although, their interpretation should be added to exploration findings (7).

  • General appearance

    Introduce yourself to the patient. Evaluate general appearance, physical state, complexity or the presence of particular face patterns, etc.

  • Head

    Inspect pupils' symmetry and reactiveness to light. Look for facial asymmetry and signs of bleeding in nostrils and oropharynx. Inspect lips, mouth and tongue, searching for lesions or signs of ulceration.

  • Neck

    Evaluate neck symmetry, venous distension and tracheal positioning. Palpate searching for adenopathies, subcutaneous emphysema, etc.

  • Thorax

    Expose the thorax, inspect the use of accessory respiratory muscles, diaphragmatic movement, and type of respiration. Also, look for ecchymosis or hematomas. Palpate searching for subcutaneous emphysema or bone crepitations. Auscultate respiratory sounds bilaterally, as well as heart sounds, noting the physiological splitting of the second heart sound, murmurs, friction and gallop rhythm or third heart sound.

  • Upper extremities

    Evaluate upper extremities symmetry. Inspect all arterial and venous line catheters. Evaluate for presence of mottled skin, peripheral pulses and perfusion through capillary filling time.

  • Abdomen

    Take into consideration the diaphragmatic movement during ventilation. Evaluate distension and tympanic sounds during the percussion of the abdomen. Palpate for any rigidity or involuntary guarding. Evaluate abnormal growth of spleen and liver, palpable masses, murmurs or other intestinal sounds.

  • Lower extremities

    Evaluate all sites of vascular accesses and palpate pulses. Evaluate mottled skin, peripheral perfusion and edema.

  • Central Nervous System and Mental State

    Evaluate if the patient is able to follow orders and if his/her four extremities can move equally. Evaluate plantar response as well as withdrawal to pain stimuli. Check pupils and facial symmetry if they were not previously evaluated.

  • Devices and Incisions

    Every possible surgical site should be evaluated, as well as the entrance of every device, including endotracheal tubes, vascular accesses, thoracic tubes, enteral probes and urinary catheters. It should be taken into consideration the characteristics and quantity of urine in the Foley bag.

  • Monitors and waveforms

    The mode, pressures, ventilation per minute and waveforms, hemodynamic monitor (venous pressure, arterial pressure), telemetry and vital signs, as well as any other type of bedside monitor, should be inspected in order to detect any qualitative or quantitative alteration/abnormality.

  • Posterior region

    Exam executed when the patient is in a prone position. Inspect looking for lesions or penetrating wounds. Pressure ulcer appearance should be evaluated.

  • Environment

    Family’s or visitors' moods should be taken into consideration. Light quality, ambient temperature, etc. should be evaluated.

Conclusions

Clinical integration of initial clinical history and the physical examination should be added to the biochemical complementation as well as advanced hemodynamic monitoring parameters, when these are available. Even so, if clinical examination answers raised questions during the initial evaluating process, the clinician must act according to physiological principles. There is no ideal hemodynamic monitoring, meaning that all parameters have to be individualized for each patient and his/her clinical context. Therefore, clinical examination systematization results are an excellent aid for the clinician regarding his/her clinical practice.  

References and Further Reading

  1. Vazquez R, Vazquez Guillamet C, Adeel Rishi M, Florindez J, Dhawan PS, Allen SE, Manthous CA, Lighthall G.  Physical examination in the intensive care unit: opinions of physicians at three teaching hospitals. Southwest J Pulm Crit Care. 2015;10(1):34-43. DOI: http://dx.doi.org/10.13175/swjpcc165-14
  2. Cook CJ, Smith GB. Do textbooks of clinical examination contain information regarding the assessment of critically ill patients?Resuscitation. 2004;60:129–136.
  3. Zehtabchi S, Kline J.A. The Art and Science of Probabilistic Decision‐making in Emergency Medicine. Academic Emergency Medicine, 17:521-523. DOI: http://doi.org/10.1111/j.1553-2712.2010.00739.x
  4. Weil MH, Shubin H. Proposed reclassification of shock states with special reference to distributive defects. Adv Exp Med Biol.1971 Oct;23(0):13-23.
  5. Ince C. The microcirculation is the motor of sepsis. Crit Care. 2005;9 Suppl 4:S13-9. DOI: 1186/cc3753
  6. Vincent JL, Ince C, Bakker J. Clinical review: Circulatory shock–an update: a tribute to Professor Max Harry Weil.Crit Care. 2012 Nov 20;16(6):239. DOI: 10.1186/cc11510.
  7. Metkus TS, Kim BS. Bedside Diagnosis in the Intensive Care Unit. Is Looking Overlooked?. Ann Am Thorac Soc.2015 Oct;12(10):1447-50. DOI: 10.1513/AnnalsATS.201505-271OI.
Cite this article as: Job Guillen, Mexico, "Clinical examination of the hemodynamically unstable patient," in International Emergency Medicine Education Project, December 6, 2019, https://iem-student.org/2019/12/06/clinical-examination-of-the-hemodynamically-unstable-patient/, date accessed: April 21, 2021

Deadly ECG Patterns – 5 Can’t Miss ECG Findings

5 Can’t Miss ECG findings

An average ER physician performs around 100 tasks in an hour and gets interrupted at least every 6 minutes. One of the common interruptions in the ED is a request to “sign off” on an ECG of a patient who has been triaged but not seen by a doctor yet. Therefore, knowing deadly ECG patterns is an essential skill for emergency physicians, residents, as well as medical students who rotate in the emergency department.

Below are five ECG patterns that should raise concerns for red flag conditions.

ECG #1

A 37-years-old female patient presented to the ED with complains of dizziness and generalized fatigue. She was started on ACE inhibitors few months ago and missed her clinic appointments. Her bedside VBG revealed a K+ of 8.1

ECG source - Dr. Smith's ECG blog

The ECG shows severe bradycardia, wide QRS complexes and symmetrically peaked T waves in V2-V5.

Key Take Home Points

Hyperkalemia can present with multiple abnormalities on an ECG, including

  • Tall, peaked T waves with a narrow base (best seen in precordial leads)
  • Progressive flattening and eventually disappearance of P waves
  • Wide QRS complexes
  • Bradyarrhythmias (sinus bradycardia, slow AF, second and third-degree AV blocks)
  • Sine wave appearance (pre-terminal rhythm)
  • Endgame: Ventricular fibrillation

Always consider the diagnosis of hyperkalemia in a patient with a history of dialysis, renal failure, or treatment with drugs like ACE inhibitors, ARBs, spironolactone especially if the ECG shows bradycardia or complete heart block.

ECG #2

A 56-years-old patient presented to the ED with lightheadedness and dizziness. Initial vitals showed hypotension and tachycardia.

ECG source - Dr. Smith's ECG blog
ECG source - Dr. Smith's ECG blog

The above ECG shows low voltage, lectrical alternans: the beat-by-beat R-wave amplitude changes best appreciated in the precordial leads. A bedside ECHO completed after the initial ECG showed a large pericardial effusion.

Key Take Home Points

Massive pericardial effusion can produce a triad of:

  • Low QRS voltage
  • Tachycardia
  • Electrical alternans (consecutive, normally-conducted QRS complexes alternate in height)

Consider the possibility of pericardial effusion and a potential impending cardiac tamponade in patients with electrical alternans on ECG.

ECG #3

A 65-years-old patient was brought to the ED by family members in a disoriented state. Further history revealed that the patient was taking digoxin as one of his regular medications. His serum digoxin level was 2.7 ng/ml.

ECG Source - learntheheart.com
ECG Source - learntheheart.com

The above rhythm strip shows atrial tachycardia with 2:1 AV block.

Key Take Home Points

Always have a high suspicion of digoxin toxicity in a patient taking digoxin presenting with the disoriented state.

Digoxin toxicity can cause a wide variety of arrhythmias. It is classically associated with supraventricular tachycardias but a slow ventricular response (e.g.: atrial tachycardia with high-grade AV block).

The other common rhythms include:

  • Regularized atrial fibrillation (AF with complete heart block + accelerated junctional escape rhythm which produces a paradoxically regular rhythm)
  • Bidirectional VT (polymorphic VT with QRS complexes alternating between LBBB and RBBB morphology)

Digoxin toxicity should be separated from the normal digoxin effect that can occur in patients taking the expected dose of digoxin. The digoxin effect (image below) includes sagging ST-segment depression, abnormal T waves (flat, inverted or biphasic) and a short QT.

ECG source - Dr. Smith's ECG blog

ECG #4

A 45-years-old patient presented to the ED with a history of severe central chest pain lasting about 10 – 15 minutes. Cardiac enzymes were negative. However, with the above ECG findings, the patient was sent to the Cath lab and subsequent coronary angiography revealed proximal LAD artery occlusion.

By Jer5150 - Own work, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=19598089

The above ECG shows deep T wave inversions in precordial leads. This is known as the Wellen’s sign.

Key Take Home Points

Wellens syndrome is a pattern of deeply inverted or biphasic T waves in V2-V3 which is highly specific for critical stenosis of left anterior descending (LAD) artery.

There are two patterns of T wave abnormality in Wellens syndrome

  • Type A: Biphasic T waves (initially positive and terminally negative)
  • Type B: Deep and symmetrically inverted (Most common type)

Note that patients can be completely pain-free with normal cardiac enzyme levels. Patients are, however, at extremely high risk of anterior wall MI due to the critical LAD stenosis and need appropriate Cardiology consultation and management urgently.

ECG #5

A 17-years-old previously healthy male patient who had one attack of syncope earlier in the day presented to the ED.

ECG Source - Peter Allely - liftl.com
ECG Source - Peter Allely - liftl.com

The ECG pattern is diagnostic of Brugada syndrome – coved shaped ST-elevation > 2mm followed by an inverted T wave seen in V1 and V2.

Key Take Home Points

Such finding is very serious in a patient with a recent episode of unconsciousness.

The suspicion of Brugada syndrome must be confirmed or excluded by an urgent consultation with a cardiologist.

Conclusion

ECGs in isolation are usually not enough to make a diagnosis – always correlate with clinical history and/or confirmatory investigations.

Try looking at as many ECGs as possible to improve your skills of pattern recognition and picking up subtle changes in ECGs.

Cite this article as: Neha Hudlikar, UAE, "Deadly ECG Patterns – 5 Can’t Miss ECG Findings," in International Emergency Medicine Education Project, November 22, 2019, https://iem-student.org/2019/11/22/deadly-ecg-patterns-5-cant-miss-ecg-findings/, date accessed: April 21, 2021