Tag: Ischemia

Transient Cerebral Ischemia (2024)

~ iEM Education Project Team ~ Leave a comment

by Omer Jaradat & Haci Mehmet Caliskan

 

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You Have A New Patient!

A 63-year-old male is brought to the Emergency Department (ED) by paramedics with a chief complaint of transient right-sided weakness. He states that the weakness started suddenly while he was watering his garden, lasted about 15 minutes, and then resolved without any residual deficits. On examination, his temperature is 36°C, blood pressure is 150/90 mmHg, pulse is 81 beats/min, respiratory rate is 18 breaths/min, and oxygen saturation is 97% on room air. 

The image was produced by using ideogram 2.0.

The patient’s past medical history is remarkable for hypertension, diabetes mellitus, and hyperlipidemia. He also smokes half a pack of cigarettes daily.

What Do You Need To Know?

Importance

Transient Cerebral Ischemia (TCI) or Transient Ischemic Attack (TIA) is defined as a sudden onset of transient, focal neurological symptoms and/or signs that occur due to focal brain, spinal cord, or retinal ischemia, without acute infarction [1]. Neurological symptoms and signs are related to the ischemic area of the brain. TIA is a neurologic emergency because patients with TIA have an early high risk of subsequent stroke. Up to 80% of strokes after TIA are preventable. Therefore, early recognition and differentiation of TIA cases are important for early treatment, which reduces the possibility of stroke. In brief, TIA represents a great opportunity for the physician to prevent stroke. Early diagnosis and treatment are the key.

Epidemiology

TIA is an important clinical condition that is common worldwide. The total global incidence of TIA is approximately 1.19 per 1000 persons per year, and it has been observed that the incidence is higher (4.88 per 1000 persons) in older age groups (85–94 years) [2]. TIA is more common in Black and male populations than in White and female populations [3].

Pathophysiology

TIA is mainly caused by three mechanisms of pathophysiology: (1) intrinsic vascular (lacunar or small vessel) pathogenesis such as atherosclerosis, lipohyalinosis, inflammation, and amyloidosis; (2) embolism originating from the heart and extracranial large vessels; and (3) low-flow conditions such as insufficient blood flow to the brain, decreased perfusion pressure, and increased blood viscosity [4].

(1) Lacunar or small vessel TIA: These TIAs are usually due to atherosclerosis of the proximal vessels or lipohyalinosis of the distal vessels. Small vessel TIAs cause symptoms similar to the lacunar strokes that are likely to follow, such as weakness or numbness in the arms, legs, and face, which are recurrent and progressive.

(2) Embolic TIAs: These are characterized by a relatively longer duration of focal neurological symptoms. These TIAs are mostly the result of embolism from a specific source. Embolism can originate from larger arteries or from the heart. In one study, it was determined that the symptoms of embolic TIAs lasted longer (hours) than those of low-flow TIAs (lasting minutes) [5].

TIAs create specific symptoms according to the regions of the occluded vessel:

  • Anterior circulation embolic TIA: Larger emboli can occlude the middle cerebral artery stem and cause contralateral hemiplegia, cortical surface symptoms (aphasia and dysexecutive syndromes in the dominant hemisphere, anosognosia or neglect in the nondominant hemisphere). Smaller emboli can occlude branches of the middle cerebral artery and cause focal symptoms such as numbness, weakness, and/or heaviness of the hand and arm.

  • Posterior circulation embolic TIA: These emboli can cause transient ataxia, diplopia, dizziness, dysarthria, hemianopsia, quadrantanopia, numbness, and unilateral hearing loss. If the embolus lodges at the top of the basilar artery, stupor or coma may occur. If the embolus lodges in the distal branches of the posterior cerebral artery, it can cause memory loss or a homonymous field defect.

(3) Low-flow TIA occurs with an obstructive vascular process in any extracranial or intracranial artery and disruption of collateral flow in the area supplied by these arteries. Low-flow TIAs are usually of short duration (minutes) and recurrent [4].

  • Anterior circulation low-flow TIA: These TIAs usually produce symptoms of a similar character. They occur due to hemodynamically significant stenotic lesions, especially in the proximal internal carotid artery, middle cerebral artery, and internal carotid artery, where collateral flow from the circle of Willis is insufficient. Ischemia-related symptoms resulting from these lesions usually include weakness or numbness in the hands, arms, legs, face, tongue, and/or cheek. Recurrent aphasic syndromes occur when there is focal ischemia in the dominant hemisphere, and recurrent neglect occurs when there is focal ischemia in the nondominant hemisphere. Limb-shaking TIAs are a rare but classic hypoperfusion syndrome in which repetitive jerking movements of the arm or leg are due to severe stenosis or occlusion of the contralateral internal carotid or middle cerebral artery.

  • Posterior circulation low-flow TIA: Unlike anterior low-flow TIA, the symptoms of these TIAs are not stereotypical because many neuronal structures in the brainstem are located very close to each other. Posterior low-flow TIA symptoms include diplopia, eyelid drooping, inability to look up, dysarthria, dizziness, drowsiness, bilateral leg and arm weakness or numbness, a feeling of heaviness, and numbness on one side of the body or face.

The diagnosis of TIA is based on the clinical features of the transient neurological attack and neuroimaging findings [6]. The majority of TIA cases do not present when fully symptomatic. For this reason, the history reported by the patient and witnesses is very important in terms of diagnosis [7]. TIA patients may experience typical or atypical symptoms.

Typical TIA:

It consists of focal neurological symptoms of sudden onset and transient character, localized to a single vascular region in the brain. These symptoms include aphasia or dysarthria, transient monocular blindness (amaurosis fugax), hemianopia, hemiparesis, and/or hemisensory loss. In such cases, the probability of ischemia is relatively high. However, these symptoms may also occur due to non-ischemic causes such as seizures, migraines, and intracerebral hemorrhage.

Atypical TIA:

Clinical characteristics of transient symptoms considered to be atypical of an ischemic attack include the following [8-10]:

  • Gradual progression of symptoms.
  • Change of symptoms from one type to another.
  • Disturbance of vision in both eyes, characterized by the occurrence of positive phenomena (positive symptoms are not normally experienced by most individuals and reflect an excess of normal functions, such as flashing lights).
  • Isolated sensory symptoms with a focal distribution, especially in areas such as a finger, chin, or tongue.
  • Attacks lasting less than 30 seconds.
  • Isolated brainstem symptoms such as dysarthria, diplopia, or hearing loss.
  • Amnesia and confusion.
  • Incoordination of limbs.

Atypical TIAs with negative symptoms (negative symptoms mean loss of a neurological function, such as hearing loss or vision loss) have a high risk of recurrent stroke. For this reason, they should be handled and treated as typical TIAs [4].

Medical History

The most important question is the time of symptom onset because it guides the treatment. Patients and/or their relatives should also be questioned about neurological diseases and symptoms (such as migraine, epilepsy, previous attacks similar to this one, syncope, etc.), cardiovascular diseases (such as myocardial infarction, atrial fibrillation, carotid stenosis, etc.), metabolic disorders (such as diabetes, hyperlipidemia, etc.), hypertension, drug usage, smoking, and family history of cardiac and/or neurological diseases.

  • Important points regarding the medical history of patients with TIA: Cardiovascular diseases, previous history of neurological attack or stroke, and drug usage.
  • Risk factors for TIA: Older age, atrial fibrillation, atherosclerosis, diabetes mellitus, hypertension, hyperlipidemia, smoking, history of stroke, male gender, and Black race.
  • Prognosis of TIA patients: The prognosis is defined by the risk of recurrent stroke. The risk of stroke after TIA varies according to several factors, including the time elapsed since the last TIA, the presence of vascular pathologies, and the presence of acute infarction on diffusion-weighted magnetic resonance imaging (DW-MRI). Stroke is most likely to occur in the first week after a TIA, with a 1.5–3.5% risk in the first 48 hours. Within 90 days, the risk of stroke rises to 40% [11–14]. Vascular pathologies such as large artery atherosclerosis, small artery disease, and cardio-embolic conditions increase the risk of recurrent stroke. Additionally, the presence of acute lesions on DW-MRI or chronic ischemic lesions on computed tomography (CT) increases the likelihood of recurrent stroke in TIA patients.

Physical Examination

A detailed neurological evaluation should be performed on the patient, including assessment of cranial nerves, strength and sensation, visual fields, language, gait, and coordination. A focal neurological deficit on exam should raise suspicion for TIA. In addition to the neurological exam, it is important to perform a thorough cardiovascular exam, listening closely for irregular rhythms, murmurs, and bruits on the carotids.

  • Red flags: Bruits on the carotids, the presence of negative symptoms, and irregular rhythms.

Alternative Diagnoses

What other diseases can present with similar clinical features/conditions?

Seizures, migraines, metabolic disorders such as hypoglycemia, subarachnoid or intracerebral hemorrhage, subdural hematoma, syncope, and central nervous system (CNS) demyelinating disorders such as multiple sclerosis, etc., should come to mind in the differential diagnosis of TIA.

Which findings make TIA more probable?

Sudden onset of typical symptoms, presence of negative symptoms, and normal laboratory and imaging findings.

Which risk factors and findings make other diagnoses more probable or make this diagnosis less probable?

We can differentiate syncope, epileptic seizures, CNS demyelinating disorders, and migraine aura with a detailed history. In the differentiation of seizures, the lactate value in an arterial blood gas (ABG) test is also important. High lactate levels support the diagnosis of seizures. Intracranial hemorrhages and subdural hematomas have specific imaging findings.

Acing Diagnostic Testing

Bedside Tests

First, vital signs (body temperature, pulse rate, respiration rate, blood pressure, and peripheral oxygen saturation) of the patient should be measured and recorded. Then, as the first approach, in all patients presenting with neurological symptoms, the measurement of blood glucose at the bedside, along with checking electrolytes, PO2, PCO2, and lactate values in an arterial blood gas (ABG) test, and performing electrocardiography (ECG), are very valuable in terms of diagnosis and differential diagnosis.

Laboratory Tests

Complete blood count (CBC), biochemistry, and coagulation tests are usually performed in addition to blood glucose measurement and ABG. These tests are useful in distinguishing metabolic disorders such as hypoglycemia from TIA. Impaired coagulation tests are also helpful in guiding diagnosis and treatment.

Imaging

Patients who are symptomatic should be considered as having a stroke. A non-contrast head CT scan can be used to assess early ischemic signs and exclude intracerebral hemorrhage. In TIA, CT has low sensitivity and usually does not show any pathological findings. If CT is negative for mass lesions and intracranial hemorrhage, computed tomography angiography (CTA) and/or magnetic resonance angiography (MRA) can be used to investigate intracranial and extracranial vascular occlusions. If CTA and/or MRA are negative for large vessel occlusion and TIA is suspected, MRI should be obtained to evaluate for signs of ischemia/infarction. DW-MRI following MRI is the gold standard for acute ischemic stroke and distinguishes stroke from TIA. DW-MRI is valuable because it shows focal areas of cytotoxic edema, which are seen in acute stroke.

Risk Stratification

The ABCD2 score (age, blood pressure, clinical features, duration, and the presence of diabetes mellitus) is commonly used to determine stroke risk following TIA. Parameters evaluated in the ABCD2 score assign scores for certain clinical features (speech impairment and unilateral weakness) and duration of symptoms, in addition to risk factors such as age, blood pressure, and diabetes. However, studies have found that the ABCD2 score does not reliably distinguish between those with a low and high risk of recurrent stroke.

Alternatively, the Canadian TIA Score uses variables routinely obtained in the ED setting to classify patients into minimal, low, high, or critical risk categories, which are associated with the likelihood of developing a stroke in the week following a TIA. Using the Canadian TIA Score strikes a balance by allowing risk stratification based on history, clinical data points, and neuroimaging, and defines clear follow-up actions based on the patient’s predictive score. Compared to the ABCD2 score, the Canadian TIA Score has shown better predictability [15].

However, there are not enough studies on the Canadian TIA Score. For this reason, a risk stratification score alone should not be used to determine the management of patients. Instead, the decision regarding hospitalization versus discharge should be made within the greater clinical context.

Management

Initial Stabilization

In all patients presenting to the Emergency Department, the initial assessment should involve the “ABCDE” approach (assessment of Airway, Breathing, Circulation, Disability, and Exposure). If the patient is alert and responds with a normal voice, the airway is open. However, if there is no respiration despite effort, the airway must be secured by checking for a foreign body, performing airway-opening maneuvers (head-tilt and chin-lift or jaw-thrust), suctioning the airway, or even intubating if necessary. In TIA patients, altered mental status is a common cause of airway obstruction [16]. If breathing is insufficient and oxygen saturation is below 94%, supplemental oxygen should be administered [17].

Altered mental status could be a sign of decreased perfusion, so obtaining intravenous access and starting IV fluids, if indicated, should be performed (the best choice is isotonic fluid). Blood pressure measurements, performing an EKG, and auscultation for abnormal heart sounds, murmurs, and carotid bruits can provide clues to the etiology of the TIA. Patients should be evaluated for disability using the Glasgow Coma Score (GCS), evaluation of pupillary light reflexes, and checking for signs of lateralization.

As hypoglycemia is considered a TIA mimic, it must be checked and corrected immediately, and hyperglycemia should also be prevented. Patients should be evaluated for drug intake and toxic ingestions. All patients with impaired consciousness should undergo a complete physical examination, which includes removing their clothes to search for signs of bleeding, foreign bodies, and trauma [16].

Medications

Treatment is started according to risk stratification.

  • If the ABCD2 score is ≥4: Dual antiplatelet therapy (DAPT) is started.

    • Aspirin (160 to 325 mg loading dose, followed by 50 to 100 mg daily) plus clopidogrel (300 to 600 mg loading dose, followed by 75 mg daily)
    • Alternatively, aspirin (300 to 325 mg loading dose, followed by 75 to 100 mg daily) plus ticagrelor (180 mg loading dose, followed by 90 mg twice daily).

  • If the ABCD2 score is <4: Aspirin monotherapy is started.

    • Aspirin (162 to 325 mg daily) [18, 19].

According to the Canadian TIA Score, patients are divided into four risk groups and managed as follows:

Minimal and Low Risk: Refer the patient to rapid outpatient assessment with a neurologist.

High Risk:

  • Start or switch to DAPT (clopidogrel or dipyridamole + ASA).
  • Initiate or control hypertension management.
  • Refer the patient to neurology within 24 hours.

Critical Risk:

  • Start or switch to DAPT (clopidogrel or dipyridamole + ASA).
  • Start oral anticoagulation if the patient has atrial fibrillation.
  • Start a statin class medication.
  • Initiate or optimize control of hypertension.
  • Admit the patient to the hospital and ensure referral to neurology within 24 hours [20].
    •  

Procedures

In patients with ongoing and disabling symptoms, emergent evaluation for IV thrombolysis and mechanical thrombectomy should be performed. Selected patients with recently symptomatic cervical internal carotid artery stenosis can significantly benefit from early carotid endarterectomy (within two weeks of a non-disabling stroke or TIA) [21].

Special Patient Groups

Stroke is a rare condition in the pediatric population, but all principles that apply to adults also apply to the pediatric population. Because the incidence of stroke increases with age, physicians should consider stroke in the management of undifferentiated geriatric patients.

In pregnant patients, physiological changes increase the risk of stroke, and there is significant maternal morbidity and mortality associated with stroke. However, a transient ischemic attack (TIA) is not a type of pregnancy-associated stroke, but it should be noted that TIAs precede strokes in up to 15% of cases [22].

When To Admit This Patient

Because of the high risk of stroke after TIA, patients diagnosed with TIA should be hospitalized for further etiological investigation and treatment.

Only selected patients with a completely normal physical examination, no ongoing disability, normal imaging (including MRI), and a low-risk score can be discharged if their neurology outpatient clinic visit is imminent and after aspirin therapy is started.

Discharged patients should be informed about TIA symptoms and encouraged to call Emergency Medical Services (EMS) and/or go to the nearest Emergency Department if these symptoms begin.

The main symptoms of a TIA can be remembered with the acronym FAST:

  • Face – Drooping or numbness on one side of the face, inability to smile, or if the mouth or eye has drooped.
  • Arms – Inability to lift both arms and keep them raised because of weakness or numbness in one arm.
  • Speech – Slurred speech, inability to talk at all despite appearing to be awake, or difficulty understanding speech.
  • Time – If any of these signs or symptoms is present, call Emergency Medical Services (EMS) immediately.

Revisiting Your Patient

The ABCDE approach was initiated as soon as the patient entered the ED. Since he is awake and does not show signs of difficulty breathing, his airway is considered open, and his breathing is considered normal.

Blood pressure is high, but pulse is within normal ranges. No murmur, abnormal sounds, or carotid murmur is detected on auscultation. Since hypoglycemia and hyperglycemia can mimic TIA, a bedside glucose level was measured and found to be 110 mg/dL (6.1 mmol/L).

A focused neurological examination was performed: pupils are equal and reactive, facial expressions appear appropriate, there is no drooping, and there is no slurring of speech. Muscle strength in his right arm is decreased, and muscle strength in his right leg is slightly decreased. There is no sensory deficit. The rest of the physical exam is unremarkable.

An electrocardiogram (EKG) was requested to check for acute pathologies and arrhythmias, such as atrial fibrillation, which is important in the etiology of TIA, and it demonstrates sinus rhythm. Since the history and physical examination are typical for an acute cerebrovascular accident, an intravenous (IV) catheter was inserted, and complete blood count (CBC), plasma urea nitrogen, creatinine, electrolytes, cardiac enzymes, and coagulation parameters (prothrombin time, activated partial thromboplastin time, and international normalized ratio [INR]) were ordered.

To exclude bleeding, the patient underwent a non-contrast brain tomography, which was interpreted as normal. The ABCD2 score was found to be ≥6. The patient was consulted with the neurology department. No focal neurological signs were detected in serial physical examinations. Thrombolytic therapy was not considered because the symptoms resolved, and the imaging was normal.

However, because the patient’s complaints were typical of stroke and/or TIA, due to comorbid diseases, and because he is not on antiplatelet therapy, he is considered to have a high risk for stroke. As a result, dual antiplatelet therapy (DAPT) was started, and the patient was transferred to the neurology service for further examination and treatment to elucidate the etiology.

Recommended Free Open Access Medical Education (FOAM) resources

  1. Zink J. (2022). Syncope and Syncope Mimics. EmDocs. Retrieved from http://www.emdocs.net/syncope-and-syncope-mimics/
  2. Chapman S. (2023). The Utility of MRI in the ED. EmDocs. Retrieved from http://www.emdocs.net/the-utility-of-mri-in-the-ed/
  3. Lanata E.P. (2021). TIA: Emergency Department Evaluation and Disposition. EmDocs. Retrieved from http://www.emdocs.net/tia-emergency-department-evaluation-and-disposition/
  4. Rezaie S. (2021). “Rebellion21: Canadian TIA Risk Score vs ABCD2”. REBEL EM blog. Retrieved from https://rebelem.com/rebellion21-canadian-tia-risk-score-vs-abcd2/

Authors

Picture of Omer Jaradat

Omer Jaradat

Dr. Omer Jaradat is an Emergency Medicine Physician at Ahi Evran University Training and Research Hospital, Kirsehir, Türkiye. He is an enthusiast of emergency medicine and strongly believes in the generalist and collective approach of the specialty. He is particularly interested in global emergency medicine, emergency medicine education, and innovation. A dedicated follower and contributor to #FOAMed, he feels proud to be a member of the emergency medicine community.

Picture of Elizabeth DeVos

Elizabeth DeVos

Dr. Haci Mehmet Caliskan is an Associate Professor of Emergency Medicine and an academician at Ahi Evran University, Kirsehir, Türkiye. He is deeply interested in emergency medicine education and is passionate about engaging students in the emergency medicine community. He is an advocate for fair and equitable medical care. His current professional interests include cardiovascular diseases, pulmonary medicine, and trauma. He takes Atatürk as an example in both his professional and social life.

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References

  1. Easton JD, Saver JL, Albers GW, et al. Definition and evaluation of transient ischemic attack: a scientific statement for healthcare professionals from the American Heart Association/American Stroke Association Stroke Council; Council on Cardiovascular Surgery and Anesthesia; Council on Cardiovascular Radiology and Intervention; Council on Cardiovascular Nursing; and the Interdisciplinary Council on Peripheral Vascular Disease. The American Academy of Neurology affirms the value of this statement as an educational tool for neurologists. Stroke. 2009;40(6):2276-2293. doi:10.1161/STROKEAHA.108.192218
  2. Lioutas VA, Ivan CS, Himali JJ, et al. Incidence of Transient Ischemic Attack and Association With Long-term Risk of Stroke. JAMA. 2021;325(4):373-381. doi:10.1001/jama.2020.25071
  3. Kleindorfer D, Panagos P, Pancioli A, et al. Incidence and short-term prognosis of transient ischemic attack in a population-based study. Stroke. 2005;36(4):720-723. doi:10.1161/01.STR.0000158917.59233.b7
  4. Rost NS, Faye EC. Definition, etiology, and clinical manifestations of transient ischemic attack. Post TW, ed. UpToDate. Waltham, MA: UpToDate Inc. http://www.uptodate.com. (Accessed on January 20, 2023.)
  5. Kimura K, Minematsu K, Yasaka M, Wada K, Yamaguchi T. The duration of symptoms in transient ischemic attack. Neurology. 1999;52(5):976-980. doi:10.1212/wnl.52.5.976
  6. Sorensen AG, Ay H. Transient ischemic attack: definition, diagnosis, and risk stratification. Neuroimaging Clin N Am. 2011;21(2):303-x. doi:10.1016/j.nic.2011.01.013
  7. Ay H, Arsava EM, Johnston SC, et al. Clinical- and imaging-based prediction of stroke risk after transient ischemic attack: the CIP model. Stroke. 2009;40(1):181-186. doi:10.1161/STROKEAHA.108.521476
  8. Fisher CM. Late-life migraine accompaniments–further experience. Stroke. 1986;17(5):1033-1042. doi:10.1161/01.str.17.5.1033
  9. Special report from the National Institute of Neurological Disorders and Stroke. Classification of cerebrovascular diseases III. Stroke. 1990;21(4):637-676. doi:10.1161/01.str.21.4.637
  10. Amarenco P. Transient Ischemic Attack. N Engl J Med. 2020;382(20):1933-1941. doi:10.1056/NEJMcp1908837
  11. Amarenco P, Lavallée PC, Labreuche J, et al. One-Year Risk of Stroke after Transient Ischemic Attack or Minor Stroke. N Engl J Med. 2016;374(16):1533-1542. doi:10.1056/NEJMoa1412981
  12. Wu CM, McLaughlin K, Lorenzetti DL, Hill MD, Manns BJ, Ghali WA. Early risk of stroke after transient ischemic attack: a systematic review and meta-analysis. Arch Intern Med. 2007;167(22):2417-2422. doi:10.1001/archinte.167.22.2417
  13. Shahjouei S, Sadighi A, Chaudhary D, et al. A 5-Decade Analysis of Incidence Trends of Ischemic Stroke After Transient Ischemic Attack: A Systematic Review and Meta-analysis [published correction appears in JAMA Neurol. 2021 Jan 1;78(1):120]. JAMA Neurol. 2021;78(1):77-87. doi:10.1001/jamaneurol.2020.3627
  14. Chandratheva A, Mehta Z, Geraghty OC, Marquardt L, Rothwell PM; Oxford Vascular Study. Population-based study of risk and predictors of stroke in the first few hours after a TIA. Neurology. 2009;72(22):1941-1947. doi:10.1212/WNL.0b013e3181a826ad
  15. Perry JJ, Sivilotti MLA, Émond M, et al. Prospective validation of Canadian TIA Score and comparison with ABCD2 and ABCD2i for subsequent stroke risk after transient ischaemic attack: multicentre prospective cohort study [published correction appears in BMJ. 2021 Feb 18;372:n453]. BMJ. 2021;372:n49. Published 2021 Feb 4. doi:10.1136/bmj.n49
  16. Thim T, Krarup NH, Grove EL, Rohde CV, Løfgren B. Initial assessment and treatment with the Airway, Breathing, Circulation, Disability, Exposure (ABCDE) approach. Int J Gen Med. 2012; 5:117-121. doi:10.2147/IJGM.S28478
  17. Piraino T, Madden M, J Roberts K, Lamberti J, Ginier E, L Strickland S. Management of Adult Patients With Oxygen in the Acute Care Setting [published online ahead of print, 2021 Nov 2]. Respir Care. 2021; respcare.09294. doi:10.4187/respcare.09294
  18. Mendelson SJ, Prabhakaran S. Diagnosis and Management of Transient Ischemic Attack and Acute Ischemic Stroke: A Review. JAMA. 2021;325(11):1088-1098. doi:10.1001/jama.2020.26867
  19. Fonseca AC, Merwick Á, Dennis M, et al. European Stroke Organisation (ESO) guidelines on management of transient ischaemic attack. Eur Stroke J. 2021; 6(2):CLXIII-CLXXXVI. doi:10.1177/2396987321992905
  20. Gladstone DJ, Lindsay MP, Douketis J, et al. Canadian Stroke Best Practice Recommendations: Secondary Prevention of Stroke Update 2020. Can J Neurol Sci. 2022;49(3):315-337. doi:10.1017/cjn.2021.127
  21. Rothwell PM, Eliasziw M, Gutnikov SA, Warlow CP, Barnett HJ; Carotid Endarterectomy Trialists Collaboration. Endarterectomy for symptomatic carotid stenosis in relation to clinical subgroups and timing of surgery. Lancet. 2004;363(9413):915-924. doi:10.1016/S0140-6736(04)15785-1
  22. Grear KE, Bushnell CD. Stroke and pregnancy: clinical presentation, evaluation, treatment, and epidemiology. Clin Obstet Gynecol. 2013;56(2):350-359. doi:10.1097/GRF.0b013e31828f25fa

Reviewed and Edited By

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.

Acute Mesenteric Ischaemia (2024)

~ iEM Education Project Team ~ Leave a comment

by Colin NG

Authors
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You have a new patient!

An 80-year-old gentleman presents to our department with a two-day history of abdominal pain accompanied by diarrhea and nausea. He describes the pain as recurrent, having occurred periodically over the past two years, with a crescendo pattern. However, this current episode has not been resolved and is excruciating.

a-photo-of-an-80-year-old-male-patient-(the image was produced by using ideogram 2.0)

A review of his medical records reveals a history of hypertension, dyslipidemia, a previous transient ischemic attack, and atrial fibrillation (AF). He underwent cholecystectomy many years ago for biliary colic. There is no other significant medical history.

On examination, his vital signs are as follows:

  • Blood pressure is 95/57 mmHg.
  • Pulse is 126 beats per minute.
  • Respiratory rate is 26 breaths per minute.
  • Oxygen saturation is 95%.
  • He is afebrile.

The patient appears pale, diaphoretic, and in significant discomfort. There is no clinical jaundice. Abdominal examination reveals diffuse tenderness, most prominent centrally, without guarding. Bowel sounds are sluggish. A cholecystectomy scar is noted in the right hypochondrium. Cardiac examination reveals irregular tachycardia, and the lungs are clear. Examination of the lower limbs is unremarkable, with no swelling. Stool is brown, with no visible blood or melena.

How would you proceed with further evaluation for this patient?

What do you need to know?

Acute mesenteric ischemia (AMI) refers to the sudden loss of blood flow to the small intestine, typically due to arterial insufficiency caused by an embolus or thrombus. AMI falls under the broader category of intestinal ischemia, which includes ischemia of the colon and, more rarely, the stomach and upper gastrointestinal tract. Other forms of intestinal malperfusion include venous occlusion as well as chronic or non-occlusive mesenteric ischemia [1].

Importance

Acute mesenteric ischemia carries an alarmingly high mortality rate, estimated between 60–80%. This is exacerbated by its nonspecific presentation, which often delays diagnosis and increases the likelihood of complications. Early recognition, timely resuscitation and treatment, and prompt advocacy for intervention are essential to improving outcomes [2,3].

Epidemiology

The incidence of AMI in developed countries is approximately 5 per 100,000 people annually, with a prevalence of around 0.1% of all hospital admissions.

AMI primarily occurs in patients with pre-existing atherosclerotic disease of arteries, often associated with risk factors such as advanced age, hypertension, diabetes, and atrial fibrillation [4].

A non-exhaustive list of risk factors includes [1]:

  • Cardiac conditions (e.g., atrial fibrillation, recent myocardial infarction)
  • Aortic surgery or instrumentation
  • Peripheral artery disease
  • Haemodialysis
  • Use of vasoconstrictive medications
  • Prothrombotic disorders
  • Systemic inflammation or infections
  • Hypovolaemic states
  • Bowel strangulation (e.g., volvulus, hernias)
  • Vascular compression syndromes.

Pathophysiology

The intestinal system exhibits relatively low oxygen extraction; residual oxygenated blood from intestinal veins is delivered to the liver via the portal vein. For ischaemic damage to occur, blood flow must be reduced by at least 50% of normal levels [1].

Interestingly, mesenteric arteries are less affected by atherosclerosis compared to other similarly sized vessels, likely due to protective hemodynamic factors. As a result, patients with AMI often have concurrent atherosclerotic conditions elsewhere, such as cerebrovascular disease, ischaemic heart disease, or peripheral vascular disease. Regarding the mechanism,

  • Embolism of the mesenteric artery accounts for ~50% and
  • Thrombosis of the mesenteric artery accounts for ~25% of AMI cases.

Mesenteric venous thrombosis can mimic AMI in a minority of cases, often presenting as nonspecific abdominal pain with diarrhea lasting 1–2 weeks. In some instances, these thrombi resolve spontaneously.

Medical History

The primary symptom of acute mesenteric ischemia (AMI) is central and severe abdominal pain, classically described as being “out of proportion” to physical examination findings. The initial pain is due to visceral ischemia, which initially spares the parietal peritoneum. Peritonism with abdominal rigidity typically develops later, indicating full-thickness ischemia, necrosis, or perforation [5].

Early symptoms may include persistent vomiting and defecation. As the condition progresses, passage of altered blood may occur. Unfortunately, associated gastrointestinal symptoms such as nausea, vomiting, and diarrhea can mimic infective causes, potentially leading to misdiagnosis. While bloody diarrhea is more commonly associated with colonic ischemia, it is less frequent in small bowel ischemia.

In some cases, AMI is preceded by symptoms of chronic non-occlusive mesenteric ischemia. Patients often report recurrent, postprandial abdominal pain resulting from an inability to increase blood flow to meet intestinal vascular demands. This may lead to a fear of eating and significant weight loss. In patients with chronic non-occlusive mesenteric ischemia, symptoms tend to be even more vague. Pain may be less severe and poorly localized, and patients may present with subtle signs such as abdominal distension or occult gastrointestinal bleeding [6].

In addition to embolic causes, mesenteric ischemia can be worsened by systemic conditions that restrict blood flow, such as hemorrhage, hypovolaemia, shock, and low-output cardiac states.

Physical Examination

In the early stages of AMI, physical examination findings are often sparse. The patient will typically appear to be in severe pain without relief, and abdominal tenderness is common. Suspicion should be heightened in frail patients of advanced age who may lack sufficient abdominal musculature to produce guarding during the examination.

Patients may appear pale due to pain or anemia, but specific physical signs are limited in this condition. Diagnosis often relies on a combination of clinical history and thorough investigation.

AMI is a critical condition characterized by reduced blood flow to the intestines, leading to severe complications if not diagnosed early. The physical examination findings should be combined with clinical history and specific symptoms. Understanding these findings is essential for timely intervention.

Key Findings

  • Severe Abdominal Pain: Patients typically present with a sudden onset of severe abdominal pain, which is a hallmark symptom of AMI.
  • Painless Interval: Following the initial pain, a transient painless period may occur, potentially misleading the diagnosis.
  • Signs of Peritonitis: Physical examination may reveal tenderness, guarding, or rebound tenderness, indicating peritoneal irritation and necessitating immediate surgical evaluation.
  • Bowel Sounds: Diminished or absent bowel sounds can suggest intestinal ischemia.

Importance of Clinical History to Guide Physical Exam

  • Risk Factors: A thorough history should include predisposing factors such as cardiovascular disease, recent surgeries, or conditions leading to hypercoagulability.
  • Chronic Symptoms: In cases of arterial thrombosis, patients may report a history of intermittent abdominal pain, weight loss, or diarrhea.

Alternative Diagnoses

The nonspecific symptoms of AMI mean it can be mimicked by many other conditions that are not easily excluded based on history and examination alone. Risk factors such as advanced age, prothrombotic states, atherosclerosis, and conditions causing hypovolaemia should raise clinical suspicion.

Differential diagnoses include:

  • Acute gastroenteritis: Main differential due to similar gastrointestinal symptoms (nausea, diarrhea, vomiting), especially at the initial stages of AMI, but pain and tenderness are typically less severe, more intermittent, and responsive to analgesia. Gastroenteritis is also less likely to cause metabolic acidosis or other significant biochemical abnormalities.
  • Acute cholecystitis: Presents with pain mainly in the right upper quadrant (RUQ) radiating to the right shoulder, often triggered by fatty meals, with accompanying nausea, vomiting, and fever. Murphy’s sign (pain and inspiratory arrest on palpation of the gallbladder) is often positive, particularly in those with a history of gallstones or biliary colic.
  • Acute pancreatitis: Epigastric pain radiating to the back, along with nausea and vomiting, is common. Associated with gallstones or alcohol use. Physical findings include epigastric tenderness, reduced bowel sounds, and, in severe cases, Grey-Turner’s or Cullen’s sign. Diagnosis is supported by elevated serum lipase or amylase levels.
  • Peptic ulcer disease: Characterized by burning or gnawing epigastric pain, often relieved by food or antacids. Common risk factors include NSAID use and Helicobacter pylori infection. Examination is typically unremarkable unless perforation occurs, which may result in acute peritonitis.
  • Bowel perforation: Sudden severe, diffuse abdominal pain with signs of peritonitis (rebound tenderness, guarding), fever, and tachycardia. A history of PUD or diverticulitis may be present. Diagnosis is supported by imaging, showing free air under the diaphragm on X-ray.
  • Diverticulitis: Presents with localized left lower quadrant (LLQ) pain, fever, and altered bowel habits (diarrhea or constipation). LLQ tenderness or a palpable mass is often noted in older patients.
  • Bowel obstruction: Crampy, intermittent abdominal pain, nausea/vomiting, abdominal distension, and constipation, potentially progressing to obstipation. Examination reveals a distended abdomen with high-pitched or absent bowel sounds. Plain X-rays typically show air-fluid levels and dilated bowel loops.
  • Ureteric calculus: Sudden colicky flank pain radiating to the groin, often with hematuria, nausea, and vomiting. A history of kidney stones is common. Findings include costovertebral angle tenderness, with a generally unremarkable abdominal exam. Hematuria is detected on urinalysis.

Acing Diagnostic Testing

Bedside Tests

Bedside diagnostics are limited but can provide valuable clues:

  • ECG: May reveal atrial fibrillation, a common risk factor.
  • Blood glucose: Hyperglycaemia due to physiological stress.
  • Point-of-Care Testing (POCT) for lactate: Elevated levels may indicate tissue hypoxia, though not specific to AMI.
  • Ultrasound: Limited in diagnosing AMI but useful for ruling out other causes of abdominal pain (e.g., cholecystitis, abdominal aneurysm, or ureteric colic). Ultrasound can also assess fluid status and response to fluid resuscitation via the inferior vena cava (IVC) and right heart function, particularly in patients with cardiac or renal comorbidities or failure.
An ECG sample in an abdominal pain patient - Rapid ventricular rate, atrial fibrillation.

Laboratory Tests

No serum markers are sufficiently sensitive or specific to diagnose AMI reliably:

  • Complete blood count (CBC): It may reveal haemoconcentration or leukocytosis but lacks specificity.
  • Serum lactate: Highly sensitive in bowel infarction but nonspecific; elevated levels may not occur in the early stages.

Leucocytosis and elevated lactate levels are the two most frequently observed abnormalities in acute mesenteric ischemia; however, both lack specificity for this condition [7,8].

  • Blood gas analysis: Metabolic acidosis is a late finding; its presence should heighten suspicion in the appropriate clinical context.
  • Serum amylase: Moderately elevated in more than half of cases; highly elevated levels suggest pancreatitis, which should guide further diagnostic steps.

Imaging

  • X-rays (Chest/Abdomen): Chest and abdominal X-rays are often normal in the early stages of acute mesenteric ischemia but are useful for identifying complications or alternative diagnoses (e.g., perforation, ureteric calculus) [9]. Early findings may include adynamic ileus, distended air-filled bowel loops, or bowel wall thickening. Late findings such as pneumatosis or portal venous gas strongly suggest bowel infarction.
  • CT Scanning: The primary imaging modality in diagnosing AMI. When enhanced with contrast, CT can detect bowel wall edema, mesenteric edema, abnormal gas patterns, intramural gas, ascites, and mesenteric venous thrombosis. Sensitivity and specificity are high (82.8–97.6% and 91.2–98.2%, respectively), though contrast use may be limited by renal function [10]. However, delaying diagnosis poses greater risks than the small chance (~1%) of contrast-induced nephropathy requiring dialysis [11].
The CT image shows bowel wall thickness.
  • Catheter Angiography: is considered the gold standard but rarely available in emergency settings [10]. It may still be necessary if CT is inconclusive and clinical suspicion remains high.
  • Diagnostic Laparotomy: it may be required for definitive diagnosis in cases of high suspicion when imaging is non-diagnostic.

Risk Stratification

No validated tools exist for risk stratification in AMI. However, specific features indicate late-stage disease and worse prognosis:

  • Prolonged symptoms before presentation.
  • Evidence of bowel necrosis or perforation.
  • Severe biochemical derangements (e.g., high lactate, metabolic acidosis).
  • Hemodynamic instability, such as septic or hemorrhagic shock.

Management

Initial Stabilization

Initial stabilization of the patient, if required, is straightforward but must follow a systematic approach, following airway, breathing, circulation, disability, and exposure.

Airway and Breathing:

The airway should be secured if necessary, especially in cases where the patient appears drowsy due to cerebral hypoperfusion or septic encephalopathy, or if they are actively vomiting and at high risk of aspiration. Rapid correction of hypovolaemia before administering sedatives or paralytics is recommended. Breathing is not commonly compromised in this condition; however, supplemental oxygen may be required for patients experiencing atelectasis or tachypnoea secondary to pain.

C: Circulation – Circulation management necessitates aggressive and rapid resuscitation with fluids or blood products. Fluid resuscitation should not be delayed due to difficulty in obtaining IV access. Ultrasound guidance can be used if venous access proves challenging. If the patient is hypotensive, an initial 10–20 mL/kg (Crystalloids: Normal saline / Hartmann’s / Ringer’s lactate / Plasmalyte etc.) bolus delivered rapidly over 5–15 minutes is appropriate. This usually requires at least one large-bore IV line (20G or larger).

Many of these patients have comorbidities such as congestive heart failure (CHF), which requires judicious fluid management. Careful hemodynamic monitoring, including repeated clinical assessments and sonographic evaluation of inferior vena cava (IVC) collapsibility, is crucial. If required, more invasive hemodynamic monitoring may be employed.

Vasoactive agents should be avoided due to their role as predisposing factors; however, if vasopressors are essential, it is advisable to avoid alpha-agonist medications.

D: Disability – In patients with acute mesenteric ischemia (AMI), mental status may become altered if ischemia progresses to sepsis or shock, leading to cerebral hypoperfusion. This may present as confusion, agitation, or lethargy. Tools such as the AVPU scale or Glasgow Coma Scale (GCS) are valuable for assessing consciousness and monitoring neurological status during treatment. Clinicians should also consider the presence of sequelae from prior strokes, as these may indicate underlying atherosclerotic disease, which is a risk factor for AMI. Additionally, severe pain can interfere with the patient’s ability to engage fully in the assessment, even when mental status remains intact.

E: Exposure – The patient should be fully exposed to enable a thorough examination, while ensuring measures are taken to maintain warmth and prevent hypothermia, as this can worsen shock. A systematic palpation of the abdomen is critical to identify tenderness, guarding, or masses. In the early stages of AMI, there may be no external signs, but central or generalized abdominal tenderness is typically present. As the condition advances, abdominal distension and signs of peritonitis, such as rebound tenderness and rigidity, may develop.

Clinicians should also observe for secondary indicators, including surgical scars or stomas, which may suggest a history of abdominal pathology. Systemic signs of hypoperfusion and shock, such as mottled skin or cool extremities, should also be noted. Regular and frequent reassessment is essential to detect any progression or subtle changes in the patient’s condition, ensuring timely and appropriate intervention.

Early and empirical administration of broad-spectrum antibiotics is critical and should not be delayed for blood culture collection, as the risk of bacterial translocation across the bowel wall is high. Oral intake must be avoided since these patients are likely to undergo urgent surgery under general anesthesia. Electrolyte imbalances should also be corrected promptly.

Antibiotic Administration

Ceftriaxone

  • Dose per kg: 1–2 g
  • Frequency: Stat (given immediately)
  • Maximum Dose: 2 g
  • Category in Pregnancy: Category B (safe for all trimesters)
  • Cautions/Comments: None specified.

Metronidazole

  • Dose per kg: 500 mg
  • Frequency: Stat (given immediately)
  • Maximum Dose: 500 mg
  • Category in Pregnancy: Category B (safe for all trimesters)
  • Cautions/Comments: None specified.

An urgent surgical consultation is imperative, as acute mesenteric ischemia is a time-sensitive condition. Delays to definitive treatment significantly increase morbidity and mortality. High clinical suspicion alone should prompt surgical involvement, even before imaging results are available. In critically ill patients, surgical teams may decide to proceed directly to the operating theatre without advanced imaging. Such decisions are typically made collaboratively by the emergency department, surgical, anesthetic, and intensive care teams.

The definitive treatment for acute mesenteric ischemia depends on the underlying cause and whether necrotic bowel is present. Necrotic bowel or signs of peritonitis necessitate immediate resection. Specific interventions include embolectomy with distal bypass grafting for mesenteric artery embolism, bypass grafting or stenting for mesenteric artery thrombosis, and removal of underlying stimuli in nonocclusive ischemia, sometimes supplemented with direct transcatheter papaverine infusion. Mesenteric venous thrombosis typically requires anticoagulation [7].

Special Patient Groups

Special populations, such as those with communication barriers or cognitive impairments, may require a lower threshold for advanced imaging since history-taking and physical examination may be unreliable. Pregnant and pediatric patients are rarely affected by this condition.

When To Admit This Patient

Given the critical nature of acute mesenteric ischemia and its high mortality rates, all affected patients should be admitted to the intensive care unit for postoperative management following surgery.

Revisiting Your Patient

Our patient was triaged to a high-acuity area of the emergency department (ED) and placed on continuous monitoring, including cardiac leads, blood pressure, and oximetry. Stabilization proceeded in a structured, prioritized manner, focusing on critical areas from A to E:

  • Airway and Breathing: The patient’s airway was intact, and there were no signs of active vomiting. Mild dyspnoea was reported, so supplemental oxygen was administered via nasal cannula.
  • Circulation: Two large-bore intravenous cannulae were inserted, and a liter of crystalloids was infused. This led to visible hemodynamic improvement, including better IVC collapsibility observed on ultrasound.
  • Disability and Exposure: Disability and exposure did not reveal anything abnormal except for a generalized tenderness on the abdomen.

With the patient stabilized, the team moved on to investigations. Blood samples were taken, including a point-of-care venous gas test with serum lactate, coagulation profile, and a group and cross-match. Leucocytes were elevated at 12,000, and serum lactate was elevated at 8. Cardiac monitoring revealed atrial fibrillation. Bedside ultrasound did not reveal other causes of abdominal pain, such as a ruptured aneurysm or cholecystitis. Chest and abdominal X-rays were normal.

Based on the clinical presentation, risk factors, and lab results, the treating team suspected acute mesenteric ischemia. A surgical consult was requested, and a CT scan of the abdomen and pelvis was ordered. Maintenance IV crystalloids and broad-spectrum antibiotics (ceftriaxone and metronidazole) were started empirically. A urinary catheter was placed to monitor fluid balance.

The CT scan revealed:

  • A thickened small bowel wall with dilated bowel loops
  • An embolism in the superior mesenteric artery

The patient was immediately taken to the operating theatre for definitive treatment.

In summary, the role of the ED physician is to:

  1. Stabilize the patient through targeted resuscitation
  2. Make an early diagnosis based on clinical suspicion supported by available investigations
  3. Understand the limitations of laboratory tests in ruling out acute mesenteric ischemia
  4. Prioritize aggressive resuscitation and management
  5. Ensure urgent surgical involvement

Authors

Picture of Colin NG

Colin NG

Woodlands Health

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References

  1. Tendler DA, Lamont JT. Overview of intestinal ischemia in adults. UpToDate. https://www.uptodate.com/contents/overview-of-intestinal-ischemia-in-adults Updated January 29, 2024. Accessed December 9, 2024.
  2. McKinsey JF, Gewertz BL. Acute mesenteric ischemia. Surg Clin North Am. 1997;77(2):307-318.
  3. Oldenburg WA, Lau LL, Rodenberg TJ, Edmonds HJ, Burger CD. Acute mesenteric ischemia: a clinical review. Arch Intern Med. 2004;164(10):1054-1062.
  4. Szuba A, Gosk-Bierska I, Hallett RL. Thromboembolism. In: Rubin GD, Rofsky NM, ed. CT and MR Angiography: Comprehensive Vascular Assessment. Philadelphia, PA, USA: Lippincott Williams & Wilkins; 2009: 295-328.
  5. Marc Christopher Winslet. Intestinal Obstruction. In: R.C.G. Russell ed. Bailey & Love’s Short Practice Of Surgery 24th ed. London, UK: Arnold; 2004:1202.
  6. Tendler DA, Lamont JT. Nonocclusive mesenteric ischemia. UpToDate. https://www.uptodate.com/contents/nonocclusive-mesenteric-ischemia Updated December 13, 2023. Accessed December 9, 2024.
  7. Park WM, Gloviczki P, Cherry KJ Jr, et al. Contemporary management of acute mesenteric ischemia: Factors associated with survival. J Vasc Surg. 2002;35(3):445-452.
  8. Cudnik MT, Darbha S, Jones J, Macedo J, Stockton SW, Hiestand BC. The diagnosis of acute mesenteric ischemia: A systematic review and meta-analysis. Acad Emerg Med. 2013;20(11):1087-1100.
  9. Smerud MJ, Johnson CD, Stephens DH. Diagnosis of bowel infarction: a comparison of plain films and CT scans in 23 cases. AJR Am J Roentgenol. 1990;154(1):99-103.
  10. Menke J. Diagnostic accuracy of multidetector CT in acute mesenteric ischemia: systematic review and meta-analysis. Radiology. 2010;256(1):93-101.
  11. Mehran R, Aymong ED, Nikolsky E, et al. A simple risk score for prediction of contrast-induced nephropathy after percutaneous coronary intervention: development and initial validation. J Am Coll Cardiol. 2004;44(7):1393-1399.

FOAM and Further Reading

CDEM Curriculum – Patel S, Mesenteric Ischemia – June 2018, https://cdemcurriculum.com/mesenteric-ischemia/ Accessed May 2023

EMdocs – Seth Lotterman. Mesenteric Ischemia: A Power Review. Nov 2014. http://www.emdocs.net/mesenteric-ischemia-power-review/ Accessed May 2023

Reviewed and Edited By

Picture of Elif Dilek Cakal, MD, MMed

Elif Dilek Cakal, MD, MMed

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.

Cardiac Monitoring (2024)

~ iEM Education Project Team ~ Leave a comment

by Stacey Chamberlain

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Definitions and Overview

Cardiac monitoring in the emergency setting is continuous monitoring of a patient’s cardiac activity in order to identify conditions that may require emergent intervention. These conditions include certain arrhythmias, ischemia and infarction, and abnormal findings that could signal impending decompensation. This chapter focuses specifically on cardiac monitoring or electrocardiography; additional methods of continuous hemodynamic monitoring in the emergency department (ED) include pulse oximetry, end-tidal CO2 monitoring, central venous pressure monitoring, and continuous arterial blood pressure monitoring. Of note, telemetry is the ability to do cardiac monitoring from a remote location; in practice, this is often a centralized system that might be located at a nursing station where multiple patients can be monitored remotely.

Cardiac monitoring differs from a 12-lead electrocardiogram in that it is done continuously over a period of time rather than capturing one moment in time in a static image. The benefit of this is that it captures transient arrhythmias and ectopic beats or monitors for changes over time. A disadvantage of cardiac monitoring is that typically, only 2 leads are displayed instead of a full 12 leads, giving a less comprehensive view of the heart and limiting its utility for looking for anatomic patterns. For example, on the 12-lead EKG, ED practitioners usually group the inferior, anterior, and lateral leads when looking for ischemic or infarct patterns. These may be less evident on a monitor with only two leads. Additionally, the static EKG allows the ED physician to carefully study it for subtle findings, for example, to make measurements of intervals, whereas in real-time monitoring, this is very difficult. In practice, both modalities are commonly used in conjunction for many ED patients.

The American Heart Association (AHA) published a consensus document in 2004 establishing practice standards for electrocardiographic monitoring in hospital settings, which was updated in 2017 [1,2]. These comprehensive documents outline the indications for cardiac monitoring, the specific skills required of the practitioner for cardiac monitoring, and specific ECG abnormalities that the practitioner should recognize. The 2017 update addressed the overuse of arrhythmia monitoring among certain populations, appropriate use of ischemia and QT-internal monitoring among select populations, alarm management, and documentation in electronic health records [2].

Cardiac monitoring is essential for those patients who are at risk for an acute, life-threatening arrhythmia and can also be used to evaluate for developing ischemia, response to therapy, and as a diagnostic tool. The AHA guidelines divide indications for cardiac monitoring in the inpatient setting into four classes based on varying degrees (level A, B, C) of evidence. Cardiac monitoring is considered indicated in patients in Class I. In Class IIa, it “is reasonable to perform” cardiac monitoring, whereas in Class IIb, it “may be considered.” For Class III, cardiac monitoring is not indicated as there is no benefit or there may actually be harm. Newer guidelines tailor the recommendations based on specific patient populations and whether the cardiac monitoring is for arrhythmia or continuous ST-segment ischemic monitoring [2]. Specific patient populations that are considered include patients with:

  1. Chest pain or coronary artery disease.
  2. Major cardiac interventions such as open heart surgery.
  3. Arrhythmias.
  4. Syncope of suspected cardiac origin.
  5. After electrophysiology procedures/ablations.
  6. After pacemaker or ICD implantation procedures.
  7. Pre-existing rhythm devices.
  8. Other cardiac conditions (acute decompensated heart failure or infective endocarditis).
  9. Non-cardiac conditions (e.g., post-conscious sedation or post-non-cardiac surgery).
  10. Specific medical conditions (e.g., stroke, imbalance of potassium or magnesium, drug overdose, or hemodialysis).
  11. DNR/DNI status.

Table 1 lists Class I-III recommendations. The AHA Scientific Statement provides a more comprehensive and detailed list.

Table 1 – Select Indications for Cardiac Monitoring

Class I Indications

Early phase ACS or after MI

 

After open-heart surgery or mechanical circulatory support

 

Atrial tachyarrhythmias

 

Symptomatic sinus bradycardia

 

2nd or 3rd degree AV block (exception as noted below for asymptomatic Wenckebach)

 

Congenital or genetic arrhythmic syndrome (e.g. WPW, Brugada, LQTS)

 

After stroke

 

With moderate to severe imbalance of potassium or magnesium

 

After drug overdose

Class IIa and IIb Indications

Non-sustained VT

 

Asymptomatic, significant bradycardia with negative chronotropic medications initiated

 

After non-cardiac major thoracic surgery

 

Chronic hemodialysis patients without other indications (e.g. hyperkalemia, arrhythmia)

Class III Indications

After non-urgent PCI without complications or after routine diagnostic coronary angiography

 

Patients with chronic atrial fibrillation, sinus bradycardia, or asymptomatic Wenckebach who are hemodynamically stable and admitted for other indications

 

Asymptomatic post-operative patients after non-cardiac surgery

 

DNR/DNI patients when the data will not be acted on and comfort-focused care is the goal

Ischemia Monitoring

Continuous ST-Segment Ischemia Monitoring was highlighted in the 2017 AHA guidelines as a specific indication for cardiac monitoring for patients most at risk for ischemia. Older monitors may not have this capability, but more modern monitors are programmed with automated ischemia monitoring that identifies abnormal ST-segment elevation or depression; manufacturers do not automatically enable this capability, and it may be turned on or off. To reduce unnecessary alarms, it is recommended (IIa level) to enable this function only in high-risk patients in the early phase of ACS and to individualize which lead should be prioritized based on the coronary artery suspected to be affected by an ischemic process. High-risk patients would include those being evaluated for vasospastic angina, those presenting with MI, post-MI patients without revascularization or with residual ischemic lesions, and newly diagnosed patients with a high-risk lesion such as a left main blockage.

QTc Monitoring

QTc monitoring aims to assess the safety of QT-prolonging medications and avoid Torsade de Pointes (TdP). Most hospitals do not have fully automated continuous QTc monitoring, so QTc monitoring and measurements may need to be performed manually or semi-automated with digital calipers. Regardless of the method, in general, recommendations for QTc monitoring are for patients with specific risk factors for TdP who are started on anti-arrhythmic drugs with a known risk for TdP (e.g., dofetilide, sotalol, procainamide, quinidine, and others), patients with a history of prolonged QTc started on non-anti-arrhythmic drugs with risk for TdP, those undergoing targeted temperature management, specific electrolyte derangements, and select drug overdoses. As with ischemic monitoring, QTc monitoring is not universally recommended for all patients, so consulting the 2017 guidelines for select patient scenarios is best.

Rhythm Interpretation

One of the most critical skills of an ED physician is in interpreting both static EKGs and interpreting arrhythmias on a cardiac monitor. A skilled practitioner must be able to diagnose common arrhythmias and be well-versed in the management of acute arrhythmias, recognizing which arrhythmias necessitate immediate action and which are less worrisome. Table 2 from the 2004 AHA guidelines lists the specific arrhythmias that the ED physician must be able to recognize. How and whether to treat an arrhythmia depends on many factors. The AHA has established algorithms for specific rhythms, including ventricular fibrillation (v-fib)/pulseless ventricular tachycardia (v-tach) and pulseless electrical activity (PEA)/asystole, as well as for non-specific rhythm categories such as bradycardia and tachycardia [3]. Additionally, they have published algorithms for clinical scenarios, including cardiac arrest, acute coronary syndrome, and suspected stroke.

The first step in the assessment of any rhythm is a clinical assessment of the patient. The premier issue of concern is if the patient is perfusing vital organs. A quick survey of the patient assessing mental status and pulses is essential to determining management. The management of a patient with v-tach will be substantially different if the patient is unresponsive and pulseless versus if the patient is awake with good pulses. As another example, the physician can quickly distinguish artifact from v-fib on the cardiac monitor by assessing the patient, as v-fib is not a perfusing rhythm.

The initial assessment of tachyarrhythmias (heart rate > 100) is to determine if the rhythm is “narrow-complex” (i.e., a QRS duration < 0.12s) or “wide-complex” (i.e., a QRS duration of 0.12s or greater). A narrow complex rhythm is considered a supraventricular rhythm (originating above the ventricles). Supraventricular tachycardia is a generic term encompassing any narrow-complex tachycardias originating above the AV node. Colloquially, when many practitioners refer to “SVT,” however, they are referring to a specific subcategory of supraventricular tachycardia called AV nodal re-entrant tachycardia (AVNRT). Wide complex tachycardias either originate in the ventricles or could originate in the atria and have an associated bundle branch block. Different criteria have been developed to help the practitioner distinguish between ventricular tachycardia and an SVT “with aberrancy” (i.e., aberrant conduction either due to an accessory path such as in Wolff-Parkinson-White or with a bundle branch block), the most well known of which are the Brugada criteria [4,5]. Practically speaking, many ED practitioners will assume the more dangerous and potentially unstable rhythm (v-tach) until proven otherwise; of course, the clinical picture and the patient’s vital signs are of utmost importance in determining the management of these patients. An excellent summary of this issue with rhythm strip examples is provided on the FOAM site “Life in the Fast Lane” [6].

Table 2 – Specific Arrythmias (adapted from AHA Scientific Statement [1])

Normal rhythms

 

 

Normal sinus rhythm

 

Sinus bradycardia

 

Sinus arrhythmia

 

Sinus tachycardia

Intraventricular conduction defects

 

 

Right and left bundle-branch block

 

Aberrant ventricular conduction

Bradyarrhythmias

 

 

Inappropriate sinus bradycardia

 

Sinus node pause or arrest

 

Non-conducted atrial premature beats

 

Junctional rhythm

AV blocks

 

 

1st degree

 

2nd degree Mobitz I (Wenckebach) or Mobitz II

 

3rd degree (complete heart block)

Asystole

 

Pulseless electrical activity (PEA)

 

Tachyarrhythmias

 

 

Supraventricular

Paroxysmal supraventricular tachycardia (AV nodal reentrant, AV reentrant)

Atrial fibrillation

Atrial flutter

Multifocal atrial tachycardia

Junctional ectopic tachycardia

Accelerated ventricular rhythm

Ventricular

Monomorphic and polymorphic ventricular tachycardia

Torsades de pointes

Ventricular fibrillation

Premature complexes

 

 

Supraventricular (atrial, junctional)

 

Ventricular

Pacemaker electrocardiography

 

 

Failure to sense

 

Failure to capture

 

Failure to pace

ECG abnormalities of acute myocardial ischemia

 

 

ST-segment elevation, depression

 

T-wave inversion

Muscle or other artifacts simulating arrhythmias

 

While each rhythm has distinctive management, it is worth noting for the novice learner that only v-fib and pulseless v-tach warrant asynchronized mechanical defibrillation (i.e. “shocking” the patient). Many students are stunned upon observing an asystolic cardiac arrest code to learn that shocking a “flatline” (i.e., asystolic) patient is an inappropriate treatment perpetuated by fictitious TV shows and movies. For unstable patients with arrhythmias but still have palpable pulses, synchronized cardioversion may be used.

Regarding medications, for certain rhythms and clinical scenarios, only vasopressor types of medications are used (e.g., epinephrine for asystole). For other rhythms and scenarios, antiarrhythmic medications are used (e.g., amiodarone for v-tach). Atrioventricular (AV) nodal blocking agents are often necessary for supraventricular tachyarrhythmias. One author suggests using a five “As” approach to treating emergency arrhythmias, keeping in mind the medications adenosine, amiodarone, adrenaline (epinephrine), atropine, and ajmaline [7]. Ajmaline is an antiarrhythmic that is not commonly used in English-speaking countries where procainamide is more common as an alternative to amiodarone for unstable v-tach.

Additional interventions may include pacemaker placement for symptomatic heart blocks. In many cases, the ED practitioner must also determine the underlying precipitant of the arrhythmia and tailor treatment to that cause. The emergency physician must familiarize himself with each rhythm and its unique management in any given clinical scenario.

At the end of this chapter, some good internet resources for the ED practitioner to practice interpreting EKGs and cardiac rhythms are provided.

Case Example

A 44-year-old male patient with a history of hypertension and end-stage renal disease on hemodialysis presents with shortness of breath after missing dialysis for 6 days. He reports gradual onset shortness of breath associated with orthopnea and increased lower extremity edema. He denies chest pain or palpitations. He does not have any cough or fever. On physical exam, he is in no distress, afebrile with a heart rate of 60, respiratory rate of 20, blood pressure of 140/78 mmHg, and oxygen saturation of 98% on room air. He has a regular rate and rhythm without murmurs and has crackles bilaterally to the inferior 1/3 of the lung bases and 1+ pitting edema of the bilateral lower extremities.

You decide to get an EKG, which shows the following:

Figure 1 (EKG from http://www.lifeinthefastlane.com)

You send a blood chemistry test, place the patient on a cardiac monitor, and one hour later note the following on the monitor:

Figure 2 - (EKG from liftl.com)

What are the indications for cardiac monitoring in this patient? What EKG abnormalities do you see? What does the rhythm strip show? What is the treatment?

Case Discussion

The ED practitioner should recognize potentially life-threatening conditions that a patient who has missed hemodialysis is at risk for are fluid overload (leading to pulmonary edema) and hyperkalemia. This patient could be considered to meet the Class I monitoring criteria for “needing intensive care” and possibly with “pulmonary edema”; however, even if the patient had no symptoms, the patient is indeed at risk for an acute life-threatening arrhythmia that would necessitate cardiac monitoring.

The EKG demonstrates peaked T waves indicative of acute hyperkalemia. Given the clinical picture of missed dialysis and the peaked Ts on the EKG, the ED physician should immediately initiate treatment for acute hyperkalemia without waiting for a confirmatory blood test (unless immediate point-of-care tests are available). If the patient’s hyperkalemia progressed, the patient could develop QRS widening with the morphology as shown on the rhythm strip called a “sine wave.” This dangerous finding could precipitously deteriorate into a life-threatening arrhythmia such as pulseless v-tach with cardiac arrest and should prompt immediate action. It is important to note that hyperkalemia can manifest in a variety of different EKG findings and does not always follow a consistent pattern from peaked Ts to QRS widening to sine waves; therefore, the patient should be treated at the first indication of any hyperkalemia-related EKG changes.

Conclusions

Cardiac monitoring is an important tool to monitor patients at risk for acute arrhythmias (including those at risk specifically for TdP) and acute or worsening cardiac ischemia. It can be helpful to immediately identify patients with life-threatening arrhythmias who need immediate intervention, to assess the response to medications for arrhythmias, and to help exclude arrhythmias as a likely etiology of a patient’s symptoms (e.g., a patient with syncope) [9]. Given the limited resources and the lack of benefits for many patients, the purpose and duration of cardiac monitoring should be carefully considered. Overuse can not only waste resources but can also contribute to alarm hazards, including “alarm fatigue,” where clinicians are barraged by so many false or nonactionable alarm signals that they become desensitized and do not respond to real events. Therefore, appropriate use and staff education are critical to maximizing the benefits of cardiac monitoring.

Author

Picture of Stacey Chamberlain

Stacey Chamberlain

Dr. Stacey Chamberlain is a board certified emergency physician who is a Professor in the Department of Emergency Medicine at the University of Illinois at Chicago (UIC). She also serves as the Director of the Global Emergency Medicine Fellowship Program and the Co-Director of the Social Emergency Medicine Fellowship Program. In addition to her work in Emergency Medicine, she is the Director of Academic Programs at the UIC Center for Global Health. In this role, she oversees the Global Medicine (GMED) Program for UIC medical students and the graduate global health certificate programs. Dr. Chamberlain has done clinical, educational, public-health, disaster-response, and emergency medicine development work, including working with several globally-focused NGOs, spanning five continents. Her global health work focuses on capacity building in emergency care in Uganda.

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2018 version of this topic – https://iem-student.org/cardiac-monitoring/

References

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  2. Sandau KE, Funk M, Auerbach A, Barsness GW, Blum K, Cvach M, Lampert R, May JL, McDaniel GM, Perez MV, Sendelbach S, Sommargren CE, Wang PJ; American Heart Association Council on Cardiovascular and Stroke Nursing; Council on Clinical Cardiology; and Council on Cardiovascular Disease in the Young. Update to Practice Standards for Electrocardiographic Monitoring in Hospital Settings: A Scientific Statement From the American Heart Association. Circulation. 2017 Nov 7;136(19):e273-e344. doi: 10.1161/CIR.0000000000000527. Epub 2017 Oct 3. PMID: 28974521.
  3. ACLS Training Center. Algorithms for Advanced Cardiac Life Support 2015. Dec 2, 2015.  Accessed at: https://www.acls.net/aclsalg.htm, Dec 10, 2015.
  4. Wellens HJJ. Ventricular tachycardia: diagnosis of broad QRS complex tachycardia. Heart2001;86:579-585 doi:10.1136/heart.86.5.579.
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  6. Burns E. VT versus SVT with aberrancy. Life in the Fast Lane. Accessed at: http://lifeinthefastlane.com/ecg-library/basics/vt_vs_svt/, Dec 10, 2015.
  7. Trappe H-J. Concept of the five ‘A’s for treating emergency arrhythmias. J Emerg Trauma Shock. 2010 Apr-Jun; 3(2): 129–136. doi:  10.4103/0974-2700.62111
  8. Ramzy M. Duration of Electrocardiographic Monitoring of Emergency Department Patients with Syncope. REBEL EM blog; June 13, 2019; Available at: https://rebelem.com/duration-of-electrocardiographic-monitoring-of-emergency-department-patients-with-syncope/.

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Reviewed and Edited By

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, vice-chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.