Question Of The Day #35

question of the day
qod35
29.2 - small bowel obstruction 2
Which of the following is the most likely cause for this patient’s condition?

This patient presents to the emergency department with generalized abdominal pain, nausea, vomiting, and constipation. The physical exam demonstrates tachycardia and a distended and diffusely tender abdomen. The patient has three prior abdominal surgeries. The upright abdominal X-ray shows multiple dilated loops of small bowel with air-fluid levels. The information provided by the history, physical exam, and diagnostic imaging collectively supports a diagnosis of small bowel obstruction.

Small bowel obstruction (SBO) is a mechanical blockage to forward flow through the intestines. The majority of SBOs are caused by post-operative scar tissue formation (adhesions), but other causes include hernias, intra-abdominal malignancies, foreign bodies, and Crohn’s disease. Symptoms include intermittent colicky abdominal pain, abdominal distension, nausea and vomiting, and constipation. Some patients may be able to pass stool and flatus early in the timeline of an SBO or if the obstruction is partial, rather than complete. Typical exam findings in SBO are a diffusely tender abdomen and high-pitched bowel sounds. Findings of abdominal rigidity, guarding, or fever should raise concern about possible intestinal perforation, peritonitis, or intestinal necrosis. Diagnosis is made clinically in combination with diagnostic imaging, such as abdominal X-rays, CT scanning, or ultrasound. CT scans have better sensitivity and specificity in diagnosing an SBO than Xray. Abdominal ultrasound is more sensitive and specific in diagnosing SBO than CT scan, but this test requires a skilled practitioner to get high-quality results. Treatment of SBO involves IV hydration, surgical consultation for possible operative intervention, pain medications, antiemetics, and electrolyte repletion. Nasogastric tube placement for gastric decompression is helpful in patients who have marked abdominal distension, intractable vomiting, or have risks for aspiration (i.e. altered mental status).

The most common cause of SBO is adhesions (Choice B), not malignancy (Choice A). Diabetic ketoacidosis (Choice C) can present with abdominal pain, nausea, and vomiting. However, DKA becomes more likely when the glucose is elevated over 250mg/dL. The presence of air-fluid levels and dilated small bowel on X-ray imaging also supports SBO over DKA. Delayed gastric emptying (Choice D) is the cause of gastroparesis, a diagnosis that can also present as nausea and vomiting. The other signs, symptoms, and imaging results make SBO a more likely diagnosis than gastroparesis.

References

Cite this article as: Joseph Ciano, USA, "Question Of The Day #35," in International Emergency Medicine Education Project, April 16, 2021, https://iem-student.org/2021/04/16/question-of-the-day-35/, date accessed: April 18, 2021

iEM Image Feed: Viscus perforation

iem image feed

A 35 years old previously healthy gentleman presented to the Emergency Department with a sudden-onset severe and diffuse abdominal pain which started an hour ago. Chest X-ray was ordered; what do you see?

Abdominal pain is one of the commonest ED presentations. Like acute MI, AAA rupture, or DKA, viscus perforation should be in our worst-case scenario list. The image shows free air under the diaphragm.

The expected hints for this type of patient are a history of peptic/duodenal ulcer disease, severe abdominal pain that patients do not want to move, and a rigid and very tender abdomen, which any palpation gives much pain to the patient. 

We need to remember that this situation is a surgical emergency. There are some steps that we need to do immediately for this patient.

  1. Proper history and examination
  2. Attaching to monitor and following vital signs and intervene if necessary to normalize them
  3. Opening 2 large-bore IV lines and fluid resuscitation as needed
  4. IV pain medication
  5. IV antibiotics
  6. Stopping oral ingestion and placing NG tube
  7. Contact surgery
  8. Sending basic biochemistry lab, coagulation profile, blood type and cross, CBC, which will be asked by surgery soon. 
  9. Arranging transfer to the OR
887.1 - viscus perforation

Abdominal pain is one of the commonest ED presentations. Like acute MI, AAA rupture, or DKA, viscus perforation should be in our worst-case scenario list. The image shows free air under the diaphragm.

887.2 - viscus perforation

The expected hints for this type of patient are a history of peptic/duodenal ulcer disease, severe abdominal pain that patients do not want to move, and a rigid and very tender abdomen, which any palpation gives much pain to the patient. 

We need to remember that this situation is a surgical emergency. There are some steps that we need to do immediately for this patient.

  1. Proper history and examination
  2. Attaching to monitor and following vital signs and intervene if necessary to normalize them
  3. Opening 2 large-bore IV lines and fluid resuscitation as needed
  4. IV pain medication
  5. IV antibiotics
  6. Stopping oral ingestion and placing NG tube
  7. Contact surgery
  8. Sending basic biochemistry lab, coagulation profile, blood type and cross, CBC, which will be asked by surgery soon. 
  9. Arranging transfer to the OR

Additional reading

Cite this article as: iEM Education Project Team, "iEM Image Feed: Viscus perforation," in International Emergency Medicine Education Project, April 14, 2021, https://iem-student.org/2021/04/14/viscus-perforation/, date accessed: April 18, 2021

GHB/GBL overdose in Recreational Settings

GHB/GBL overdose in Recreational Settings

GHB and GBL are two drugs of abuse frequently used as stimulants at parties for various reasons. Acute intoxication quickly leads to coma, respiratory depression, cardiac arrest and death.

One of the usage of these agents is for psychoactive substances in sexual contexts. With respect to jargon, we speak of Party and Play (PNP). Psychoactive substances are taken both recreational purposes and because they reduce self-control and inhibitions, they act as a sexual enhancer. In some cases, gamma hydroxybutyrate/gamma butyrolactone (GHB/GBL) mixed with alcoholic drinks facilitate criminal actions, such as robbery or non-consensual sexual acts (date rape drugs).Use of these drug is not very common in the general population and can be ascribed to distinct user groups[1].

What are the psychoactive substances most used in these parties?

The most frequent psychoactive substances used these parties are usually five:

  • GHB (gamma hydroxybutyrate)
  • GBL (gamma-butyrolactone)
  • Cathinones (Mephedrone, methylenedioxypyrovalerone [MDPV], methylone)
  • Methamphetamine
  • Ketamine

However, concomitant use of other abuse drugs [2], such as cocaine, ethanol, benzodiazepines, cannabinoids, and methamphetamines, can lead to the more significant severity of poisoning caused by GHB/GLB.

What are the effects of GHB?

GHB is a drug used in liquid or powder form. In liquid form, it is a clear, salty, and odorless. GHB is gamma aminobutyric acid (GABA) sodium salt, a molecule present in many body tissues; it is linked to GABA neurotransmitters, which are inhibitory to the neurons to which it binds. It activates its receptors (GHB receptors) and also activates GABA-B receptors [3]. Binding of GHB o to the latter group of receptors leads to a release of dopamine in the brain and causes the depression of the central nervous system (CNS), which can lead to decreased consciousness or unconsciousness, especially when ingested together with other depressants, such as alcohol.

From a pharmacological point of view, GHB has a narrow therapeutic range. At low doses (20–30 mg/kg), it produces a euphoric effect. Higher doses (> 50 mg/kg) provoke a sedative–hypnotic effect, which can further induce coma, bradycardia, and hypoventilation. Absorption into the body is relatively fast (5–15 min.) With a relatively short half-life, the peak of plasma concentrations occurs after 20 to 45 min. The clinical symptoms and the duration of the symptoms are dose-dependent so that it is almost not present in the body after 4 to 6 hours.

Structural formula of GBL
Structural formula of the chemical compound gamma-hydroxybutyrate (from Wikipedia – Neurotiker – Public Domain)
Metabolic pathway of GBL and GHB.
Metabolic pathway of 1,4-butanediol, GBL and GHB. (from Wikipedia-Anypodetos – Public Domain)

What are the effects of GBL?

GBL is a liquid product of the chemical industry. GBL differs from GHB because it has a chemical smell and acid taste, but after ingestion, our body converts GBL to GHB. Compared to GHB, we have seen how GBL has faster absorption, a longer-lasting effect, and higher plasma concentrations. These characteristics indicate quicker absorption and explain how GBL intake rapidly evolves toward an overdose characterized by coma, respiratory depression, cardiac arrest, and death. The pharmacodynamics of GBL are even faster than those of GBH.

2D structure of GBL (from Wikipedia-Harbin – Public Domain)

What are the symptoms of GHB / GBL overdose?

Symptoms of GHB / GBL overdose include several features:

  • Unconsciousness (GCS 3–7)
  • Reduced consciousness (narcolepsy, cataplexy)
  • Psycho-motor agitation
  • Cardio-circulatory problems (bradycardia, hypotension)
  • Respiratory depression
  • Seizures

How to diagnose GHB/GBL overdose?

The diagnosis of acute GBL and GHB intoxication is clinical. The symptoms include two main forms of depression:

  • CNS depression
  • Respiratory depression

GHB/GBL blood or urine tests are not always available in all hospital settings, while diagnostic confirmation through chromatography or mass spectrometry takes several days. Obtaining a patient’s medical history is difficult, if not impossible, due to his/her altered mental state or coma onset. However, the discovery of bottles and participation in a rave/nightclub event can help recreate the events and form the clinical picture.

What to do in front of a patient with a GBL/GHB overdose?

Treatment of the patient suffering from a GBL/GBH overdose is primarily supportive. The patient should be monitored via pulse oximetry, cardiorespiratory monitoring, capnography, and temperature monitoring.

The patient’s airway should be protected and the patient should be managed conservatively (if possible). Ways to treat the airways are highly debated and are currently left to the treating physician’s discretion.  Intubation [4] should be avoided in the patient which he used only GHB as the half-life of this drug is extremely short, and the patient could awaken in 2 to 3 hours. On the other hand, if poly-intoxication is present, the patient is in critical condition, or there is a real risk of aspiration pneumonia, intubation should be performed. It should also be remembered that GBL is a highly inflammatory molecule for the upper respiratory tract tissues.

Atropine or catecholamines if the perfusion is not adequate should be used, but this event is rare in these patients.Moreover, the onset of the withdrawal symptoms [5] such as anxiety, insomnia, tremors, tachycardia, agitation, delirium, and hallucinations should be monitored and treated with benzodiazepines and muscle relaxants [6].

What are the other risks?

Patients who inject drugs via the intravenous route should be informed of the risk of contracting infectious diseases [7], such as human immunodeficiency virus, hepatitis C and B viruses (HIV, HCV, and HBV, respectively). Those on retroviral therapy should be notified that these agents decrease the effectiveness of antiretroviral drugs [8].

The patient should be informed that taking GBL/GHB with other drugs can lead to severe and potentially fatal conditions. It should be remembered that GHB and cocaine mixed with alcohol react by forming toxic metabolites, such as cocaethylene, or that GHB and opioids can lead to coma and death.

The patient who is dependent on GHB should be informed about the onset of withdrawal symptoms, which is of rapid onset and progression and can often be fatal as hallucinatory, delusional, upon sudden drug cessation. Epileptic seizures can occur and can endanger a patient’s life. Planning for reductions in GHB/GBL use before stopping altogether can reduce withdrawal symptoms and make them less severe. If a person is  a regular user of one or more of these drugs, a doctor should be consulted before discontinuing use as sudden withdrawal can be life-threatening. Also, withdrawal symptoms can last up to 15 days.

Useful links

References and Further Reading

  1. Tomkins A, Ahmad S, Cannon L, Higgins SP, Kliner M, Kolyva A, Ward C, Vivancos R. Prevalence of recreational drug use reported by men who have sex with men attending sexual health clinics in Manchester, UK. Int J STD AIDS. 2018 Mar;29(4):350-356. doi: 10.1177/0956462417725638. Epub 2017 Aug 23. PMID: 28835196.
  2. Madah-Amiri, D., Myrmel, L. & Brattebø, G. Intoxication with GHB/GBL: characteristics and trends from ambulance-attended overdoses. Scand J Trauma Resusc Emerg Med 25, 98 (2017). https://doi.org/10.1186/s13049-017-0441-6
  3. Le JK, Richards JR. Gamma-Hydroxybutyrate Toxicity. [Updated 2020 Oct 21]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK430781/
  4. P Dietze, D Horyniak, P Agius, V Munir, de Villiers Smit, J Johnston, C L Fry, L Degenhardt. Effect of intubation for gamma-hydroxybutyric acid overdose on emergency department length of stay and hospital admission Acad Emerg Med2014 Nov;21(11):1226-31
  5. Wojtowicz JM, Yarema MC, Wax PM. Withdrawal from gamma-hydroxybutyrate, 1,4-butanediol and gamma-butyrolactone: a case report and systematic review. CJEM 2008; 10:69–74
  6. Cappetta M, Murnion BP. Inpatient management of gamma-hydroxybutyrate withdrawal. Australas Psychiatry. 2019 Jun;27(3):284-287. doi: 10.1177/1039856218822748. Epub 2019 Jan 17. PMID: 30652947.
  7. Sewell, Janey et al. Poly drug use, chemsex drug use, and associations with sexual risk behaviour in HIV-negative men who have sex with men attending sexual health clinics. International Journal of Drug Policy 43, 33–43, 2017
  8. Pufall, EL et al. Sexualized drug use (‘chemsex’) and high-risk sexual behaviours in HIV-positive men who have sex with men, HIV medicine 19.4, pp. 261–270, 2018
Cite this article as: Francesco Adami, Italy, "GHB/GBL overdose in Recreational Settings," in International Emergency Medicine Education Project, April 12, 2021, https://iem-student.org/2021/04/12/ghb-gbl-overdose/, date accessed: April 18, 2021

Question Of The Day #34

question of the day
qod34

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

This patient is pregnant in the first trimester presenting to the Emergency department with right lower quadrant pain. Any first trimester pregnant patient with abdominal pain should be evaluated for ectopic pregnancy. Other causes of this symptom include ovarian torsion, ovarian cyst rupture, pelvic inflammatory disease, tubo-ovarian abscess, urinary tract infection, ureterolithiasis, colitis, or appendicitis. An intra-uterine pregnancy is confirmed on transvaginal ultrasound which excludes ectopic pregnancy from the differential. Ovarian pathologies are also investigated on the ultrasound and are not discovered. 

Another common diagnosis based on the patient’s pain location, young age, and markedly tender abdomen is acute appendicitis. The most common presenting symptom in appendicitis is right lower quadrant pain. Other signs include fever, anorexia, nausea, or vomiting.  Pregnant women may present with back or flank pain, rather than right lower quadrant pain, as the uterus may displace the appendix in the abdomen. There is no single symptom or laboratory test that can reliably exclude the diagnosis of appendicitis. The gold standard test for acute appendicitis diagnosis is a CT scan of the abdomen with IV contrast dye. PO or PR contrast are additionally used in some institutions based on preference and protocols.  In children, appendiceal ultrasound is performed first to avoid excessive radiation exposure and financial cost. CT scanning (Choice A) is similarly avoided in first-trimester pregnancy to diagnose appendicitis, although it is the test of choice in non-pregnant adults. MRI imaging of the abdomen and pelvis (Choice C) is another diagnostic option for pregnant patients, but this is not recommended until an ultrasound is performed. IV antibiotics (Choice D) may be needed to treat appendicitis or other abdominal infections, but this patient lacks a definitive diagnosis or signs of sepsis or shock which would support emergent antibiotics. The best next step to further evaluate the cause of this patient’s symptoms is conducting an appendiceal ultrasound (Choice B). If this study is non-conclusive or is not available, an MRI should be performed. 

Emergency department treatment for acute appendicitis is IV antibiotics, IV hydration, and surgical consultation for appendectomy. Immediate surgery may be avoided in patients who present several days after symptom onset or with a ruptured appendix. These cases are treated with IV antibiotics, IV hydration, bowel rest, and close monitoring.

References

Cite this article as: Joseph Ciano, USA, "Question Of The Day #34," in International Emergency Medicine Education Project, April 9, 2021, https://iem-student.org/2021/04/09/question-of-the-day-34/, date accessed: April 18, 2021

iEM Image Feed: Plateau Fracture

iem image feed

A 60-year-old man known to have DM type 2 was brought by the family as a camel hit his knee. He was not able to walk on it at the scene and in ED. It was swollen with no open wound.

Tips
Although patients come with isolated injuries, we always have to make sure that they do not have other injury findings. Therefore, approaching systematically to the patient is important. At this moment, please remember primary and secondary surveys of multiple trauma. The animal attacks may create multiple injuries on patients, and they should be evaluated as multiply injured patients. After you ruled our multiple or life, organ, extremity threatening injury, you can deep dive into isolated injuries. In this case, knee injury after a direct hit.

Of course, inspection and palpation are essential in every extremity injury. Evaluating the patient for neurovascular problems and range of motions are applied in almost every extremity trauma. But sometimes, clinical presentations or findings can be subtle and you may need a better tool. In these case, we recommend using Ottawa Knee Rules.

The image shows tibia plateau fracture on AP knee x-ray.

885.1 plateau fracture
885.2 plateau fracture copy

Additional reading

Cite this article as: iEM Education Project Team, "iEM Image Feed: Plateau Fracture," in International Emergency Medicine Education Project, April 7, 2021, https://iem-student.org/2021/04/07/plateau-fracture/, date accessed: April 18, 2021

Illness Narratives In Global Health

Storytelling is a powerful tool that allows us to relate to one another across borders, cultures, and experiences. It is a significant aspect of global health. Images associated with international health are those of pediatric patients in low and middle-income countries (LMICs) with descriptions of ailment or news stories on television of an outbreak in a faraway country. These stories capture our attention and allow us to process situations far removed from ours. While stories allow us to communicate the urgency and extent of international health topics, there are challenges associated with illness narratives. It is important to examine how stories are told in medicine, and specifically in global health. It is critical to question who tells stories, how they’re told, and what their impact is. These can be stories of individual patients in a country, medical aid organizations, or even stories of a country’s health infrastructure.

A recent Lancet essay titled “Global Health 2021: Who tells the Story” examines the role of journals when it comes to research in academic global health. The essay cites data showing a lower number of publications authored by those affiliated with or came from LMIC in The Lancet Global Health(1). Here, the authors reflect on how, as a London-based global health journal, they need to examine the narration disparities. They note that an imbalance in authorship is a symptom of an imbalance in power when it comes to academic global health.

This essay was in part motivated by a crucial article by Seye Abimola and Madhukar Pai. In their article examining the decolonization of global health, Abimola and Par state “even today, global health is neither global nor diverse. More leaders of global health organisations are alumni of Harvard than are women from low-income and middle-income countries. Global health remains much too centred on individuals and agencies in high-income countries (HICs).”(2) This important point highlights the distance between the subject of stories and those who tell them. This can limit diversity in perspective while taking away ownership of stories from those who experience it.

An article looking at illness narratives in an outbreak reported that when it comes to Ebola, Zika, and SARS, marginalized communities often bear the burden of disease while their account of illness is often neglected. The authors state, “regardless of income setting, there is a need to give voice to the most marginalized communities during an epidemic.”(3) This point on narration should extend beyond authorship in research to include news coverage of global health events. The way the Ebola outbreak and even early days of COVID pandemic were portrayed are examples of the dangers associated with lack of nuance in the way global health topics are discussed in the media.

Inclusivity of illness narratives around global health can allow us to avoid pitfalls that lead to widespread misinformation and discrimination. In addition to examining who tells the story, it is also important to explore how stories are told. An essay highlighting the challenges of storytelling in medicine notes that at times the trauma of subjects has been exploited by international charities. The article states the importance of communicating stories in a way that does not “feast on the trauma of others”(4). 

At the core of his argument is the need to examine how we communicate the stories of others. As described above, allowing locals to tell stories regarding their experience of illness, outbreaks, and research can help us deal more carefully with the associated trauma. Stories told without careful consideration can lead to widespread misinformation and potentially harmful generalizations. As we move towards examining how we improve global health delivery, it is critical to explore how we can improve the stories we share. In order to create a better system to communicate important global health topics, it is imperative to challenge the ways we receive information constantly.

This will broaden our understanding of complex issues and allow us to consider alternative solutions.

To this end, the following five questions should help us navigate the challenges of global storytelling. These questions are suggested to help guide our approach towards a more

  1. Has the subject given informed consent to tell their story?
  2. How is the story presented?
  3. Is there a way to allow the story subject to be
  4. Do the stories told reinforce harmful stereotypes?
  5. Are there negative consequences to the subject if the story is told?

References and Further Reading

  1. Health TLG. Global health 2021: who tells the story? The Lancet Global Health. 2021;9(2):e99.
  2. Abimbola S, Pai M. Will global health survive its decolonisation? The Lancet. 2020;396(10263):1627-1628.
  3. Kapiriri L, Ross A. The politics of disease epidemics: a comparative analysis of the sars, zika, and ebola outbreaks. Glob Soc Welf. 2020;7(1):33-45.The
  4. Harman S. The danger of stories in global health. The Lancet. 2020;395(10226):776-777
Cite this article as: Nardos Makonnen, USA, "Illness Narratives In Global Health," in International Emergency Medicine Education Project, April 5, 2021, https://iem-student.org/2021/04/05/illness-narratives-in-global-health/, date accessed: April 18, 2021

Question Of The Day #33

question of the day
qod33
AAA CT scan possible rupture

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

This elderly male patient presents to the emergency department with abdominal pain. Compared to younger patients, abdominal pain in an elderly patient has a higher likelihood of being due to a surgical emergency or from a diagnosis that carries a higher mortality. Elderly patients may have more nonspecific associated symptoms that may make it difficult to confirm a dangerous diagnosis without advanced imaging. Additionally, elderly patients do not always have a fever or elevated white blood cells during an abdominal infection. The differential diagnosis of abdominal pain in an elderly patient should be broad and encompass conditions related to many body systems.

The syncopal event and signs of shock should raise concern for a more serious etiology of the patient’s symptoms. The CT image provided shows a dilated aorta filled with contrast dye and a large surrounding intra-luminal thrombus. An infrarenal abdominal aorta measuring over 3cm is considered aneurysmal. This patient’s abdominal aorta measures approximately 7cm from outer wall to outer wall using the scale provided on the right-hand side of the image. The green measurement line in the image below shows the size of the aorta from outer wall to outer wall (includes thrombus).

The diagnosis for this patient is a ruptured abdominal aortic aneurysm (AAA). This condition carries a high mortality and is often lethal without prompt surgical intervention (Choice A). Administration of blood products is helpful if there are signs of hemorrhagic shock as in this patient. Antibiotics, like IV Vancomycin and Piperacillin-Tazobactam (Choice B), are not helpful in the management of this diagnosis. Endotracheal intubation (Choice C) is needed prior to operative intervention, but Emergency department management should focus on volume resuscitation and close communication with the surgical team for operative repair. IV Heparin (Choice D) may be beneficial in acute mesenteric ischemia from an embolic etiology (i.e. Atrial fibrillation), but anticoagulation would worsen this patient’s hemorrhagic shock.

AAAs can present to the Emergency department without any symptoms and be discovered incidentally on imaging or on physical exam as a pulsatile abdominal mass. Other presentations include severe back pain (the abdominal aorta is retroperitoneal) and circulatory shock. Rupture of a AAA can be large and result in rapid decompensation and death, or bleeding can be contained in the retroperitoneal space with transiently stable vital signs. Risk factors for AAA formation are male sex, tobacco use, hypertension, increased patient age, Marfans syndrome, or Ehlers-Danlos syndrome. The diagnosis of AAA is clinical and includes the use of bedside aortic ultrasound or CT aortic angiogram imaging. Treatment for AAA depends on aortic size and patient symptoms. Operative repair is indicated for any AAA over 5.5cm diameter in men, over 5.0cm diameter in women, or any size if there are signs of shock or concern for AAA rupture.

References

Cite this article as: Joseph Ciano, USA, "Question Of The Day #33," in International Emergency Medicine Education Project, April 2, 2021, https://iem-student.org/2021/04/02/question-of-the-day-33/, date accessed: April 18, 2021

iEM Image Feed: Radius and Ulna Fracture

iem image feed radius and ulna fracture
radius and ulna fracture

Her father brought a 9-year-old girl due to deformed right extremity. He was playing at home and fell from a hight on his hand. No open wounds. No past medical and surgical. Vaccination: up to date.

Examination: radial pulse is intact. He can move the fingers but with limitation due to pain. Sensation is normal. The X-ray showed both radius and ulna fracture. The patient underwent procedural sedation with IV ketamine, and the reduction was made with ortho oncall.

Cite this article as: iEM Education Project Team, "iEM Image Feed: Radius and Ulna Fracture," in International Emergency Medicine Education Project, March 31, 2021, https://iem-student.org/2021/03/31/radius-and-ulna-fracture/, date accessed: April 18, 2021

Organophosphate poisoning

Organophosphate poisoning

Introduction

  • Organophosphate compounds can be commonly found in insecticides and are associated with systemic illness.
  • Mortality is higher in developing countries where organophosphate pesticides are more commonly available.
  • Organophosphorus poisoning can result from occupational, accidental, or intentional exposure.
  • Its use as a suicidal agent is frequent.
  • The primary cause of death in acute organophosphate poisoning is bradyasystolic arrest from respiratory failure.

Pathophysiology

Organophosphate compounds bind irreversibly to acetylcholinesterase inactivating the enzyme through the process of phosphorylation and acetylcholine at nerve synapses and neuromuscular junctions. Thus, it results in overstimulation of acetylcholine receptors.

Clinical presentation

Here are a few mnemonics for the Muscarinic Effects of Cholinesterase Inhibition: SLUDGE, DUMBELS, and Killer B’s (Figure 1 & 2).

SLUDGE - DUMBELS
Killer B's
  • Out of four distinct syndromes that can occur from organophosphate poisoning, the first two are clinically important in emergency setting 1. Acute poisoning, 2.intermediate syndrome, 3.chronic toxicity, and 4.organophosphate induced delayed neuropathy. Of these syndromes, the intermediate syndrome is the most feared one as it presents with paralysis of the neck’s flexor muscles, muscles innervated by the cranial nerves, proximal limb muscles, and respiratory muscles. It occurs up to 40% of poisonings within 1 to 5 days of initial symptoms.
  • Acute organophosphate poisoning can present with differing severities. Mild poisonings generally present with symptoms like lightheadedness, nausea, headache, dyspnea, lacrimation, rhinorrhea, salivation, and diaphoresis while moderate poisonings cause autonomic instability, confusion, vomiting, muscle spasms, bronchorrhea and bronchospasm. Coma, seizures, flaccid paralysis, urinary and fecal incontinence, and respiratory arrest may occur in the course of severe poisonings.
  • Diagnosis is based on history (people may bring bottles/substance itself) in the presence of a suggestive toxidrome. Cholinesterase assays and reference laboratory testing for specific compounds may confirm the diagnosis but take time and have limitations. Treatment should be started without delay based on the clinical findings.
  • Miosis (papillary constriction) and muscle fasciculation are the most reliable signs of organophosphate toxicity and help in diagnosis.

Treatment

  • The first step of the treatment is decontamination. Healthcare workers must wear protective equipment to avoid secondary poisoning. The patient should be decontaminated with ample water and soap preferably before arriving in a hospital or once stable. Water should be disposed of as hazardous waste.
  • In addition to decontamination, treatment consists of airway control, intensive respiratory support, general supportive measures, prevention of absorption, and the administration of antidotes.
  • The patient should be monitored continuously and provided 100% oxygen. Gastric lavage and activated charcoal are not recommended.
  • A non-depolarizing agent should be used when the neuromuscular blockade is needed during intubation since succinylcholine is metabolized by plasma butyrylcholinesterase, and therefore, may prolong paralysis.
  • The specific agents are atropine and Atropine can be given repeatedly every 5 minutes until tracheobronchial secretions attenuate (1-3 mg IV in adults or 0.01-0.04 mg/kg IV in children – never <0.1 mg per dose). Then, a continuous infusion should be started to maintain the anticholinergic state (0.4-4 mg/h in adults).
  • Pralidoxime is the single most important treatment for the nicotinic effect of organophosphate poisoning and is life-saving for intermediate syndrome if used within 48 hours (First dose: 1-2 g in adults or 20-40 mg/kg – up to 1 g – in children, mixed with NS and infused over 5-10 min, continuous infusion: 500 mg/h in adults or 5-10 mg/kg/h in children)
  • Seizures can be treated with benzodiazepines.

Disposition and follow-up

  • Minimal exposures may require only decontamination and 6 to 8 hours of observation in the ED to detect delayed effects.
  • Admission to the intensive care unit is necessary for significant poisonings.
  • Most patients respond to pralidoxime therapy with an increase in acetylcholinesterase levels within 48 hours.
  • The endpoint of therapy is the absence of signs and symptoms after withholding pralidoxime therapy.
  • Death from organophosphate poisoning usually occurs in 24 hours in untreated patients, usually from respiratory failure secondary to paralysis of respiratory muscles, neurologic depression, or bronchorrhea.

References and Further Reading

  1. Burillo-Putze, G. & Xarau S. N. “Pesticides. Tintinalli JE, Stapczynski JS, Ma OJ, Yealy DM, Meckler GD, Cline DM, editors. Tintinalli’s emergency medicine: a comprehensive study guide 8th ed.” (2016): 1318-25.
  2. Katz K. D. & Brooks D. E. “Organophosphate Toxicity Treatment & Management” Medscape, Dec 31, 2020, https://emedicine.medscape.com/article/167726-treatment. Accessed Feb 05, 2021.
Cite this article as: Temesgen Beyene, Ethiopia, "Organophosphate poisoning," in International Emergency Medicine Education Project, March 29, 2021, https://iem-student.org/2021/03/29/organophosphate-poisoning/, date accessed: April 18, 2021

Question Of The Day #32

question of the day
qod32

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

This patient has intermittent epigastric abdominal pain with nausea and vomiting that radiates to the back. He has a history of alcohol abuse, but lacks tremors or tongue fasciculations to demonstrate signs of active alcohol withdrawal. Laboratory testing reveals pre-renal acute kidney injury (BUN/Creatinine ratio >20), elevated liver function tests with a hepatocellular pattern (AST>ALT in 2:1 ratio), and a markedly elevated lipase.  This information supports a diagnosis of acute pancreatitis. Administration of IV midazolam, a benzodiazepine, would be an appropriate next step if the patient had signs or symptoms of alcohol withdrawal. Alcohol withdrawal can begin as early as 6 hours after refraining from alcohol intake in a chronic alcohol user.  Information regarding alcohol intake is not provided in the question, but objective clinical signs indicating withdrawal are not present on exam. Ordering a CT scan of the abdomen and pelvis (Choice B) is not required in making the diagnosis of acute pancreatitis.  A CT scan can be helpful if you are considering an alternative diagnosis (i.e. AAA, abdominal abscess, etc) or if there is concern for sepsis or fulminant pancreatitis. 

 

Diagnosis of pancreatitis is made clinically based on the history and physical exam, risk factors for the disease, and laboratory testing.  Pancreatitis typically presents as upper abdominal pain that radiates to the flanks and back.  Nausea and vomiting are frequent accompanying symptoms. The disease can range from mild symptoms to severe symptoms with pancreatic necrosis, multi-organ failure, shock, and Acute Respiratory Distress Syndrome (ARDS). Serum lipase testing is more specific than amylase for pancreatitis. Lipase is elevated in pancreatitis.  Risk factors for the disease include gallstones, alcohol use, abdominal trauma, recent ERCP, hypertriglyceridemia, pancreatic ischemia, scorpion envenomation, certain viral infections (Mumps, CMV), hypercalcemia, and certain medications (sulfonamides, azathioprine, valproic acid, etc).  The most common cause of first-time pancreatitis is gallstones. A gallbladder ultrasound should always be performed in patients with a gallbladder who present with pancreatitis. A surgical consultation (Choice C) for gallbladder removal would be warranted if this patient had gallstone pancreatitis, but the patient has a history of a cholecystectomy. The likely cause of this patient’s pancreatitis is his alcohol abuse which causes direct pancreatic injury and inflammation. Treatment of pancreatitis includes IV hydration (Choice D), analgesia, antiemetics, and monitoring for electrolyte abnormalities. Avoiding food or liquid intake (NPO) for “pancreatic rest” has been recommended historically for all cases of pancreatitis, however there is not robust evidence to support this practice.  Routine antibiotics are not recommended for acute pancreatitis, unless there are signs of sepsis.

References

Cite this article as: Joseph Ciano, USA, "Question Of The Day #32," in International Emergency Medicine Education Project, March 26, 2021, https://iem-student.org/2021/03/26/question-of-the-day-32/, date accessed: April 18, 2021

The Future of Resuscitation in the ED: ECMO-CPR (Part 2)

ecmo-cpr 2
Part 2 of this post continues with the use of ECMO during CPR. To learn more about ECMO, here is the link to Part 1

What is E-CPR?

E-CPR is defined as the utilization of veno-arterial extracorporeal membrane oxygenation (V-A ECMO) in patients who experience a sudden and unexpected pulseless condition secondary to the cessation of cardiac mechanical activity.

Rationale for E-CPR

The idea of E-CPR originated due to deficiencies in conventional CPR (C-CPR), which, even under optimal conditions, only delivers 15-25% of normal cardiac output. This leads to rapid hypoperfusion and ischemic damage to vital organs (what is known as the low-flow state). However, E-CPR is able to supply near-normal levels of organ perfusion; therefore, preserve the brain and other vital organs for days or weeks until cardiac recovery takes place.

In addition, E-CPR facilitates coronary interventions, even in patients with sustained ventricular fibrillation, because V-A ECMO provides stable systemic perfusion. Therefore, E-CPR has been considered a way to buy tome for the subsequent diagnosis and treatment of the underlying cause of cardiac arrest. Moreover, it provides better survival rates and neurologic outcomes.

Indications and patient selection for E-CPR

Up to date, there are no universal inclusion criteria for E-CPR. Inclusion criteria commonly used in E-CPR studies are the following:

  • Patients aged 18 to 65 or 18 to 70 years
  • Witnessed refractory cardiac arrest
  • Immediate bystander CPR
  • Initial shockable rhythm
  • Access to immediate coronary angiography
  • An anticipated low-flow period <60 minutes

Other common inclusion criteria for E-CPR include signs of life and end-tidal CO2 level >10 mm Hg on arrival to the emergency department. Their value in E-CPR is yet to be systematically assessed.

When should the transition to E-CPR occur?

No consensus is available regarding the ideal time to switch from C-CPR to E-CPR. Starting E-CPR too early may predispose patients who could potentially recover without it to a complicated and expensive procedure. On the other hand, delaying E-CPR may take away the core benefit of the intervention, which is, reducing low-flow state time and organ ischemia.

Studies showed that after 35 minutes of C-CPR, only less than 1% of patients achieve ROSC with good neurological outcomes. One study revealed that 16 minutes after the initiation of C-CPR by emergency medical services might be the optimal time to proceed to E‐CPR. Another study showed superior neurological outcome with the transition after 21 minutes in selected patients. However, delivering patients to a hospital within ab appropriate time frame presents a challenge to EMS staff. Prehospital E-CPR provides an alternative solution to this challenge.

Outcomes of C-CPR versus E-CPR:

Up to date, no published randomized controlled trial compared C-CPR versus E-CPR. Most of the evidence comes from retrospective and prospective observational studies, and meta-analysis. These studies included patients with out-of-hospital cardiac arrest (OHCA) and in-hospital cardiac arrest (IHCA). For example, the SAVE-J study, a prospective observational study, revealed that patients with OHCA who underwent E-CPR had a better neurological outcome, measured by a cerebral performance category of 1 or 2, compared to those with C-CPR, at 1 month (12.3% vs 1.5%, P<0.0001) and at 6 months (11.2% vs 2.6%, P=0.001). Kim et al. also reported favourable neurological outcomes at 3 months in the E-CPR group. Moreover, some recent systematic reviews have demonstrated trends that link E-CPR with improved survival and neurologic outcomes. Overall, factors that were associated with better outcomes included young age, witnessed arrest, bystander CPR, rhythm of sustained VF/VT, time from OHCA to E-CPR initiation, and acute coronary syndrome.

The latest study regarding E-CPR for OHCA was published in June 2020. It took place in Paris and included 13.191 OHCA cases. Of the 12,396 patients managed with C-CPR, 1061 (8.6%) survived to hospital discharge, compared with 44 (8.4%) of 523 E-CPR patients. E-CPR was attempted but failed in 58 (11%) patients. Factors associated with survival in the E-CPR group included an initial shockable rhythm and transient return of spontaneous circulation (ROSC) prior to E-CPR. This study posed major questions regarding the effectiveness of E-CPR in patients with OHCA. The fact that there was no statistical difference between C-CPR and E-CPR made the science community to realize the need to reevaluate the literature and for more and larger randomized clinical trials.

Prehospital E-CPR:

Pre-hospital ECMO aims to reduce the time to E-CPR initiation and increase potential positive outcomes (Figure 2). A cohort performed in Paris attempted to initiate E-CPR after 20 minutes of failed C-CPR and within 60 minutes of arrest. Outcomes revealed reduced low-flow state by 20 minutes and improved survival with neurologically intact patients up to 29% (21% absolute increase, P<0.001). This concluded that prehospital E‐CPR reduced low‐flow duration significantly and increased the rate of ROSC, but it was not an independent predictor of survival to discharge.

APACAR2 (A Comparative Study Between a Pre‐hospital and an In‐hospital Circulatory Support Strategy (ECMO) in Refractory Cardiac Arrest), an ongoing promising RCT, is randomizing patients with OHCA to either prehospital or hospital E‐CPR groups, depending on their location and predicted transport time to the hospital. It will reveal more about E-CPR use in the prehospital setting.

Limitations and closing remarks:

Current evidence concerning the effectiveness of E-CPR seems low quality, making drawing strong conclusions on OHCA E-CPR impossible. Additionally, positive outcomes may be associated with the whole “E-CPR bundle of care”, which include rapid hospital transfer, C-CPR and coronary angiography. Consequently, the effectiveness of E-CPR on its own is uncertain and more RCTs are needed.

Lastly, the survival rate of approximately 25-30% with E-CPR for IHCA already represents a huge financial and resource burden to the family and healthcare systems. If survival with OHCA E-CPR is potentially less than 10%, is it worth the burden or should we better invest in reducing cardiovascular morbidity and improve conventional bystander CPR?

prehospital ecmo-cpr
Figure 2: Prehospital ECMO (Ref: 11 - Nickson, C. (2020). Extracorporeal Membrane Oxygenation. Accessed Feb 26, 2021, from https://litfl.com/ecmo-extra-corporeal-membrane-oxygenation/)
Cite this article as: Amani Khalouf, UAE, "The Future of Resuscitation in the ED: ECMO-CPR (Part 2)," in International Emergency Medicine Education Project, March 24, 2021, https://iem-student.org/2021/03/24/ecmo-cpr-part-2/, date accessed: April 18, 2021

References and Further Reading

  1. Berdowski, J., Berg, R. A., Tijssen, J. G., & Koster, R. W. (2010). Global incidences of out-of-hospital cardiac arrest and survival rates: systematic review of 67 prospective studies. Resuscitation, 81(11), 1479-1487.
  2. Bougouin, W., Dumas, F., Lamhaut, L., Marijon, E., Carli, P., Combes, A., … & Jouven, X. (2020). Extracorporeal cardiopulmonary resuscitation in out-of-hospital cardiac arrest: a registry study. European Heart Journal, 41(21), 1961-1971.
  3. Dennis, M., Lal, S., Forrest, P., Nichol, A., Lamhaut, L., Totaro, R. J., Burns, B., & Sandroni, C. (2020). In-Depth Extracorporeal Cardiopulmonary Resuscitation in Adult Out-of-Hospital Cardiac Arrest. Journal of the American Heart Association, 9(10), e016521.
  4. Gräsner, J. T., Lefering, R., Koster, R. W., Masterson, S., Böttiger, B. W., Herlitz, J., … & Zeng, T. (2016). EuReCa ONE-27 Nations, ONE Europe, ONE Registry: A prospective one month analysis of out-of-hospital cardiac arrest outcomes in 27 countries in Europe. Resuscitation, 105, 188–195.
  5. Grunau, B., Reynolds, J., Scheuermeyer, F., Stenstom, R., Stub, D., Pennington, S., … & Christenson, J. (2016). Relationship between time-to-ROSC and survival in out-of-hospital cardiac arrest ECPR candidates: when is the best time to consider transport to hospital?. Prehospital Emergency Care, 20(5), 615-622.
  6. Hutin, A., Abu-Habsa, M., Burns, B., Bernard, S., Bellezzo, J., Shinar, Z., … & Lamhaut, L. (2018). Early ECPR for out-of-hospital cardiac arrest: best practice in 2018. Resuscitation, 130, 44-48.
  7. Hutin, A., Loosli, F., Lamhaut, L., Mantz, B., & Corrocher, R. (2017). How Physicians Perform Prehospital ECMO on the Streets of Paris. Accessed Feb 26, 2021, from https://www.jems.com/patient-care/how-physicians-perform-prehospital-ecmo-on-the-streets-of-paris/
  8. Inoue, A., Hifumi, T., Sakamoto, T., & Kuroda, Y. (2020). Extracorporeal Cardiopulmonary Resuscitation for Out‐of‐Hospital Cardiac Arrest in Adult Patients. Journal of the American Heart Association, 9(7), e015291.
  9. Kim, S. J., Jung, J. S., Park, J. H., Park, J. S., Hong, Y. S., & Lee, S. W. (2014). An optimal transition time to extracorporeal cardiopulmonary resuscitation for predicting good neurological outcome in patients with out-of-hospital cardiac arrest: a propensity-matched study. Critical Care, 18(5), 1-15.
  10. MacLaren, G., Masoumi, A. & Brodie, D. (2020). ECPR for out-of-hospital cardiac arrest: more evidence is needed. Critical Care24, 7
  11. Nickson, C. (2020). Extracorporeal Membrane Oxygenation. Accessed Feb 26, 2021, from https://litfl.com/ecmo-extra-corporeal-membrane-oxygenation/
  12. Singer, B., Reynolds, J. C., Lockey, D. J., & O’Brien, B. (2018). Pre-hospital extra-corporeal cardiopulmonary resuscitation. Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine, 26(1), 1-8.
  13. Tan, B. K. K. (2017). Extracorporeal membrane oxygenation in cardiac arrest. Singapore Medical Journal, 58(7), 446.

The Future of Resuscitation in the ED: ECMO-CPR (Part 1)

ecmo-cpr 1

As a junior emergency department (ED) physician, I clearly remember my first code -first cardiopulmonary resuscitation (CPR) attended- and the mixed feelings of sorrow and helplessness for not being able to bring that soul back to life despite our best efforts. After a couple of more codes, listening to the sounds of the hearts slowly fading away, my mind started to question: How effective is the current standard Advanced Cardiac Life support (ACLS) protocol we follow?

I remember admitting to one of my attendings how desperate I felt about the ACLS during every code, expecting very abysmal neurological and overall outcomes, even if the patient was lucky enough to achieve the return of spontaneous circulation (ROSC). It almost felt that what we did was completely futile. A couple of weeks later, during my cardiology rotation, I had a field trip in the cardiac intensive care unit (ICU) with one of the cardiologists who introduced me to different advanced mechanical support devices, including extracorporeal membrane oxygenation (ECMO), intra-aortic balloon pump (IABP) and others. While he explained the basic concepts behind how they functioned, it almost immediately occurred to me: “Well! That’s what we need in cardiac arrest patients!”

While certainly, it was not a very novel idea, it did urge me to search into the available evidence and where we stood in terms of bringing this idea into more practical terms. This is how I was introduced, as a postgraduate year one (PGY-1) ED resident, to the concept of ECMO-CPR.

What is ECMO?

Extracorporeal membrane oxygenation (ECMO) is the use of a blood pump and an oxygenator to support either pulmonary or both pulmonary and cardiac function. An ECMO circuit is usually made of a centrifugal pump and a membrane oxygenator for oxygen delivery, CO2 removal, and temperature management.

What are the types of ECMO?

There are two main types of ECMO circuits:

Veno-venous (V-V) ECMO

Veno-venous (V-V) ECMO provides lung support only so it requires a functional heart. Venous cannulae are usually placed in the right or left common femoral vein (for drainage) and right internal jugular vein (for infusion). The tip of the femoral cannula should be maintained near the junction of the inferior vena cava and right atrium, while the tip of the internal jugular cannula should be maintained near the junction of the superior vena cava and right atrium.

Veno-arterial (V-A) ECMO

Veno-arterial (V-A) ECMO provides both cardiac and pulmonary support. The drainage (access) cannula is placed into the inferior vena cava via the femoral vein, and the “return” cannula is inserted into the femoral artery to the level of the common iliac artery.

We will focus on V-A ECMO given its relation with E-CPR.

How does V-A ECMO work?

Venous blood (blue) drained via a cannula positioned at the inferior vena cava to the right atrial junction passes through the extracorporeal membrane where oxygenation and CO2 removal occurs. The oxygenated blood (red) is returned via a “return” cannula positioned in the common iliac artery or descending aorta. After ECMO support is established, the distal perfusion catheter is inserted into the superficial femoral artery distal to the insertion point of the femoral return cannula, and it supplies oxygenated blood to the distal limb to prevent distal limb ischemia (Figure 1).

ecmo-cpr
Figure 1: V-A ECMO Configuration (Ref: 3 - Dennis, M., Lal, S., Forrest, P., Nichol, A., Lamhaut, L., Totaro, R. J., Burns, B., & Sandroni, C. (2020). In-Depth Extracorporeal Cardiopulmonary Resuscitation in Adult Out-of-Hospital Cardiac Arrest. Journal of the American Heart Association, 9(10), e016521.)

What are the indications for VA-ECMO?

  • Cardiac arrest
  • Low Cardiac Index (<2L/min/m2) and hypotension despite inotropic support and an IABP.
  • Failure to wean from cardiopulmonary bypass
  • Cardiogenic shock or severe cardiac failure, caused by:
    • Acute coronary syndrome
    • Ventricular tachycardia storm or refractory arrhythmias.
    • Sepsis
    • Drug overdose/toxicity
    • Myocarditis
    • Massive pulmonary embolism
    • Cardiac trauma
    • Acute anaphylaxis

What are the contraindications for VA-ECMO?

The list below includes both absolute and relative contraindications:

  • Patients with non-recoverable cardiac dysfunction who are not candidates for left ventricular assist device (LVAD) or transplantation
  • Chronic organ dysfunction
  • Prolonged CPR without adequate tissue perfusion
  • Disseminated malignancy
  • Known severe brain injury
  • Unwitnessed cardiac arrest
  • Contraindications to therapeutic-dose anticoagulation
  • Severe aortic regurgitation
  • Aortic dissection
  • Existent multiorgan failure
  • Mechanical ventilation >7–10 days
  • Advanced age

We will continue with the use of ECMO during CPR in the part 2. Stay tuned!

Cite this article as: Amani Khalouf, UAE, "The Future of Resuscitation in the ED: ECMO-CPR (Part 1)," in International Emergency Medicine Education Project, March 22, 2021, https://iem-student.org/2021/03/22/ecmo-cpr-part-1/, date accessed: April 18, 2021

References and Further Reading

  1. Berdowski, J., Berg, R. A., Tijssen, J. G., & Koster, R. W. (2010). Global incidences of out-of-hospital cardiac arrest and survival rates: systematic review of 67 prospective studies. Resuscitation, 81(11), 1479-1487.
  2. Bougouin, W., Dumas, F., Lamhaut, L., Marijon, E., Carli, P., Combes, A., … & Jouven, X. (2020). Extracorporeal cardiopulmonary resuscitation in out-of-hospital cardiac arrest: a registry study. European Heart Journal, 41(21), 1961-1971.
  3. Dennis, M., Lal, S., Forrest, P., Nichol, A., Lamhaut, L., Totaro, R. J., Burns, B., & Sandroni, C. (2020). In-Depth Extracorporeal Cardiopulmonary Resuscitation in Adult Out-of-Hospital Cardiac Arrest. Journal of the American Heart Association, 9(10), e016521.
  4. Gräsner, J. T., Lefering, R., Koster, R. W., Masterson, S., Böttiger, B. W., Herlitz, J., … & Zeng, T. (2016). EuReCa ONE-27 Nations, ONE Europe, ONE Registry: A prospective one month analysis of out-of-hospital cardiac arrest outcomes in 27 countries in Europe. Resuscitation, 105, 188–195.
  5. Grunau, B., Reynolds, J., Scheuermeyer, F., Stenstom, R., Stub, D., Pennington, S., … & Christenson, J. (2016). Relationship between time-to-ROSC and survival in out-of-hospital cardiac arrest ECPR candidates: when is the best time to consider transport to hospital?. Prehospital Emergency Care, 20(5), 615-622.
  6. Hutin, A., Abu-Habsa, M., Burns, B., Bernard, S., Bellezzo, J., Shinar, Z., … & Lamhaut, L. (2018). Early ECPR for out-of-hospital cardiac arrest: best practice in 2018. Resuscitation, 130, 44-48.
  7. Hutin, A., Loosli, F., Lamhaut, L., Mantz, B., & Corrocher, R. (2017). How Physicians Perform Prehospital ECMO on the Streets of Paris. Accessed Feb 26, 2021, from https://www.jems.com/patient-care/how-physicians-perform-prehospital-ecmo-on-the-streets-of-paris/
  8. Inoue, A., Hifumi, T., Sakamoto, T., & Kuroda, Y. (2020). Extracorporeal Cardiopulmonary Resuscitation for Out‐of‐Hospital Cardiac Arrest in Adult Patients. Journal of the American Heart Association, 9(7), e015291.
  9. Kim, S. J., Jung, J. S., Park, J. H., Park, J. S., Hong, Y. S., & Lee, S. W. (2014). An optimal transition time to extracorporeal cardiopulmonary resuscitation for predicting good neurological outcome in patients with out-of-hospital cardiac arrest: a propensity-matched study. Critical Care, 18(5), 1-15.
  10. MacLaren, G., Masoumi, A. & Brodie, D. (2020). ECPR for out-of-hospital cardiac arrest: more evidence is needed. Critical Care24, 7
  11. Nickson, C. (2020). Extracorporeal Membrane Oxygenation. Accessed Feb 26, 2021, from https://litfl.com/ecmo-extra-corporeal-membrane-oxygenation/
  12. Singer, B., Reynolds, J. C., Lockey, D. J., & O’Brien, B. (2018). Pre-hospital extra-corporeal cardiopulmonary resuscitation. Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine, 26(1), 1-8.
  13. Tan, B. K. K. (2017). Extracorporeal membrane oxygenation in cardiac arrest. Singapore Medical Journal, 58(7), 446.