Tag: stroke

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.

Intracerebral Hemorrhage (2024)

~ iEM Education Project Team ~ Leave a comment

by Muhammad I. Abdul Hadi, Iskasymar Ismail, Kamarul Baharuddin, and Erin Simon

Authors
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You have a new patient!

A 60-year-old female was brought to the Emergency Department (ED) with a complaint of sudden onset of left-sided body weakness associated with facial asymmetry and vomiting. She was known to have hypertension. On arrival, she was drowsy with a Glasgow Coma Scale of 13/15 (E3, V4, M6). Her pupils were equal and reactive. 

The image was produced by using ideogram 2.0.

Her vital signs were as follows: blood pressure 210/118 mmHg, heart rate 96 beats per minute, respiratory rate 20 breaths per minute, oxygen saturation 98% on room air, and afebrile. Her left upper limb and lower limb examination showed hyperreflexia and reduced motor power to 0/5. Her left plantar response was extensor. Her right upper and right lower limbs were unremarkable. Capillary blood sugar was 9.3 mmol/L.

What is your differential diagnosis and outline your management?

What do you need to know?

Importance

Altered mental status (AMS) is a neurological emergency with many differential diagnoses. A general approach to AMS is to look for structural or metabolic causes. The most common structural cause of AMS is an acute stroke. Stroke can be classified into two major categories: ischemic and hemorrhagic. Hemorrhagic stroke can be further divided into two types: intracerebral hemorrhage (ICH) and subarachnoid hemorrhage [1]. ICH is associated with poor functional outcomes and carries high morbidity and mortality. In addition, most patients who survive an ICH have disabilities and cognitive decline and are at risk for recurrent stroke.

Patients with ICH can present with an abrupt onset of focal neurological signs. The clinical features typically evolve over minutes to a few hours. However, in subarachnoid hemorrhage, the symptoms are typically maximal at onset [2]. Depending on the volume of the hemorrhage, location, and the extent of the affected brain tissue, the patient may experience vomiting, headache, hemiparesis, hemisensory loss, facial weakness, aphasia, dysarthria, visual disturbance, and AMS when the hemorrhage is significant. However, the patient may not have those typical symptoms if the hemorrhage is small and in an uncommon site.

Signs of significant elevation of intracranial pressure (ICP) due to mass effect or herniation from ICH are:

  • Unequal pupil size
  • Dilated pupils
  • Comatose
  • Cushing triad (bradycardia, respiratory depression, hypertension)

Epidemiology

ICH is a neurological emergency case that is frequently encountered in ED. It is the second leading cause of stroke, accounting for up to 27 percent of all stroke cases globally. There are over 12.2 million new strokes each year, and 6.5 million people die from stroke annually. The risk of developing a stroke in a lifetime is one in four people over age 25 [3].

Pathophysiology

The pathophysiology of spontaneous ICH depends on its etiologies. These include hypertensive vasculopathy, cerebral amyloid angiopathy, aneurysms, arterio-venous malformations (AVM), cerebral venous thrombosis, hemorrhagic infarction, reversible cerebral vasoconstriction syndrome, cerebral vasculitis, sickle cell disease, anticoagulation therapy, and bleeding disorder [2]. 

Common sites for ICH and its common presentation include [4]:

  • Basal ganglia (40-50%): contralateral hemiplegia, gaze preference to the side of bleeding
  • Lobar regions (20-50%): Focal neurologic deficits; hemiparesis, hemisensory loss, and gaze preferences
  • Thalamus (10-15%): contralateral hemiplegia, gaze preferences away from the  side of bleeding
  • Brainstem (5-12%): impaired loss of consciousness, pinpoint pupils, cranial nerve palsies, absent or impaired horizontal gaze, and facial weakness
  • Cerebellum (5-10%): vertigo, vomiting, and limb ataxia

Medical History

Spontaneous ICH frequently presents with acute onset of stroke symptoms, such as acute focal neurological deficits (limb weakness and slurred speech), AMS, and features of increased intracranial pressure (vomiting and headache). The presence of AMS, vomiting, and headache are the essential features to differentiate hemorrhagic from ischemic stroke. AMS occurs in approximately 50% of the cases. In addition, neurological symptoms may develop during routine activity, exertion, or intense emotional activity. However, these symptoms may be absent with small hemorrhages [2]. Seizures may also develop if the hemorrhages involve cortical or cerebellar tissue.

Risk Factors for ICH

Risk factors for ICH can be simplified with the mnemonic of ABCDEFGH.

A: Age (elderly, the risk of ICH increases with advancing age) and alcohol consumption – Heavy alcohol use is associated with an approximately threefold increased risk of ICH

B: Blood pressure (hypertension) – the most important risk factor. This results in small vessel damage to deeper structures such as the basal ganglia and thalamus.

C: Cigarette smoking – In the Physicians Health Study, active smokers had a relative ICH risk of 2.06 percent compared with non-smokers 

D: Drug (antiplatelet, anticoagulant, and stimulant drug abuse) – Anticoagulation (warfarin) increases the risk of ICH two to fivefold. Stimulant drugs have been associated with a risk of ICH due to possible spikes in blood pressure and vasospasm.

E: Exercise and healthy lifestyle – Inactivity and obesity are comorbidities that can lead to increased risk for ICH

F: Family history

G: Gender (ICH is more prevalent in men than women) and race (Black Americans have a higher risk than White Americans). Asian countries have a higher incidence of ICH than other regions [4].

H: Hypo/hypercholesterolemia – A systematic review and meta-analysis found that low cholesterol was associated with an increased ICH risk

Others:

  • Cerebral Amyloid Angiopathy- Risk increases with age. Amyloid protein deposition weakens vessels’ structural integrity.
  • Structural Abnormalities- aneurysms, connective tissue diseases, congenital AVMs, and family history of subarachnoid hemorrhage (SAH) increase ICH risk.

Physical Examination

The physical examination of a patient with ICH begins with ensuring the stability of airway, breathing, and circulation. Once stabilized, a thorough neurological examination is performed. On inspection, the patient may present with an altered sensorium, ranging from drowsiness to stupor or coma, along with hemiparesis or hemiplegia, with hemiplegia being more common. Facial asymmetry may also be observed.

The general examination should assess for high blood pressure and risk factors such as nicotine stains on fingernails, indicative of smoking, or signs of alcoholic liver disease. Using the ABCDEFGH approach for risk factor identification is advised.

The specific neurological examination typically reveals deficits that correspond to the site of the hemorrhage and the associated edema. Cranial nerve abnormalities may manifest as unequal pupil size, visual field defects, ptosis, facial asymmetry, dysphasia, and a reduced gag reflex. Nuchal rigidity may be noted. Examination of the motor system often shows features of upper motor neuron (UMN) lesions, such as hemiplegia, hypertonia, hyperreflexia, and a positive Babinski sign. Sensory examination may reveal hemisensory loss, while involvement of the cerebellar system can present as sudden, severe vertigo accompanied by akinesia.

An assessment of other systems is essential to identify risk factors and complications associated with ICH. The cardiovascular system may show signs of stress-induced cardiomyopathy or acute cardiac failure. The respiratory system should be evaluated for complications like aspiration pneumonia. Examination of the lower limbs may reveal venous thrombotic events, and systemic signs like fever and infections should also be assessed.

Progressive elevation of intracranial pressure (ICP) or herniation is associated with several clinical features that require immediate attention. Pupillary changes are commonly observed, including impaired reactivity to light, which may indicate worsening neurological status. Abducens nerve (cranial nerve VI) palsy can also occur, with alert patients potentially reporting horizontal diplopia. Additionally, progressive altered mental status (AMS) is a hallmark of increasing ICP. In more advanced stages, the Cushing triad, characterized by bradycardia, respiratory depression, and severe hypertension, may manifest as a critical sign of impending herniation.

Alternative Diagnoses

When evaluating a patient for ICH, it is essential to consider alternative diagnoses and inquire about specific risk factors. Acute ischemic stroke or transient ischemic attack (TIA) can present similarly to ICH and require neuroimaging for differentiation. A history of trauma may suggest a traumatic head injury, such as an epidural or subdural hematoma. Cerebral abscess should be considered if there is a history of fever, headache, and focal neurological deficits. Similarly, meningitis or encephalitis may present with fever, photophobia, neck stiffness, and seizures. A brain tumor often has a subacute to chronic onset with headache and focal neurological signs. Drug overdose or toxin-induced states warrant a thorough review of the patient’s medication and substance history. Metabolic disturbances, such as uremic encephalopathy or renal failure, and acute hypoglycemia or hyperglycemia, should also be considered. Post-epileptic paralysis (Todd’s paralysis), complicated migraine or hemiplegic migraine, and hypertensive encephalopathy are other important differential diagnoses that must be ruled out based on clinical history and investigations.

Acing Diagnostic Testing

Bedside Tests

In the evaluation of patients with suspected intracranial events, capillary blood sugar is a critical bedside test. Random blood glucose measurement helps exclude hypoglycemia or hyperglycemia, as hypoglycemia, in particular, can mimic stroke-like symptoms. Rapid identification and correction of blood glucose abnormalities are essential for accurate diagnosis and appropriate management.

Laboratory Tests

Several laboratory tests provide critical diagnostic insights. A full blood count is essential, as leukocytosis may indicate infection or infarction, lymphocytosis is associated with viral meningitis, and neutrophilia suggests bacterial meningitis. Thrombocytopenia may point toward a bleeding tendency. Renal function tests measuring urea and creatinine are crucial for identifying renal failure, while liver function tests are important in patients suspected of having liver disease. Measurement of INR helps identify coagulopathies, which may increase bleeding risk. Additionally, an arterial blood gas test is indicated in cases of respiratory distress to assess for respiratory failure or metabolic disorders.

Electrocardiogram (ECG)

ECG changes in patients with intracranial conditions can include a prolonged QT interval and ST-T wave changes. These findings may indicate catecholamine-induced cardiac injury [5], which is a potential complication in such cases.

Toxicology Screening

Toxicology screening is essential when drug poisoning or alcohol use is suspected in a patient. Plasma and urine samples should be sent for toxicology analysis to identify potential toxic substances, aiding in diagnosis and guiding appropriate treatment.

Imaging

Imaging plays a crucial role in the evaluation of ICH. A non-contrast head CT is the first-line modality for accurately identifying acute ICH, where a hyperdense lesion can be observed. It is also effective in ruling out other conditions such as brain tumors, cerebral metastasis, skull fractures, hydrocephalus, cerebral ischemia, and cerebral abscess. In addition, a CT angiogram can detect underlying causes like aneurysms or vascular malformations and is recommended for patients under 70 years old to assess for vascular origins of ICH [4].

While both MRI and CT are equally effective in detecting acute ICH, MRI is superior for identifying chronic ICH [4]. In cases with large vessel occlusions, CT may be used; however, for patients with an NIH stroke scale score >6 and a normal head CT, thrombolytic therapy may be considered after consultation with a stroke neurologist and evaluation of contraindications. Although MRI offers greater accuracy for acute strokes, its use in the emergency department is limited by time and availability.

Finally, a chest X-ray is helpful for identifying complications such as pulmonary edema or consolidation caused by aspiration or pneumonia, which may occur alongside intracranial events.

The Image Archieve of Intracranial Hemorrhage on iEM

Risk Stratification

The ICH score is extensively used as a clinical grading scale and communication tool to estimate subsequent 30-day mortality and decide on the appropriate care option [6]. It is commonly used in conjunction with the FUNC (Functional Outcome in Patients with Primary Intracerebral Hemorrhage) score, which predicts the functional independence of ICH patients after 90 days [7].

ICH score

The ICH Score, ranging from 0 to 6, is a clinical grading system developed by to predict outcomes in ICH patients [6]. Points are assigned based on specific criteria: one point for age over 80 years, one point for an infratentorial origin of the hemorrhage, one point for an ICH volume exceeding 30 ml, one point for intraventricular extension of the hemorrhage, one point for a Glasgow Coma Scale (GCS) score between 5 and 12, and two points for a GCS score of 3 or 4. This scoring system provides a standardized approach to assessing the severity of ICH.

  1. Glasgow Coma Score (GCS score of 5-12 = 1, GCS score of 3 or 4 = 2) 
  2. Age ≥80 = 1
  3. Presence of ICH volume ≥30 mL = 1
  4. Presence of intraventricular hemorrhage = 1
  5. Presence of infratentorial origin of hemorrhage = 1

In the ICH score, 1 point corresponds to a 13% mortality rate, 2 points to 26%, 3 points to 72%, 4 points to 97%, and 5 or more points indicate a 100% mortality rate.

FUNC score

As previously mentioned, The FUNC score is a clinical tool utilized at hospital admission to estimate the probability of achieving functional independence (defined as a Glasgow Outcome Score of 4 or higher) within 90 days after an ICH. The FUNC score includes categories below. 

  • ICH Volume (cm³):
    • Less than 30 cm³: +4 points
    • 30–60 cm³: +2 points
    • Greater than 60 cm³: 0 points
  • Age:
    • Younger than 70 years: +2 points
    • 70–79 years: +1 point
    • 80 years or older: 0 points
  • ICH Location:
    • Lobar: +2 points
    • Deep: +1 point
    • Infratentorial: 0 points
  • GCS Score:
    • Score of 9 or greater: +2 points
    • Score of 8 or less: 0 points
  • Pre-ICH Cognitive Impairment:
    • No cognitive impairment: +1 point
    • Yes, cognitive impairment present: 0 points

Functional independence is defined as a Glasgow Outcome Score of 4 or higher. According to the score interpretation, patients with a FUNC Score of 0–4 have a 0% chance of achieving functional independence. A score of 5–7 corresponds to a 29% among survivors. For a score of 8, the likelihood rises to 48%. Patients scoring 9–10 have a 75% chance to have independence. The highest score of 11 corresponds to a 95% likelihood of functional independence among survivors.

Management

The initial treatment goals for ICH are focused on preventing secondary brain damage [8]. These include preventing hemorrhage expansion, monitoring for and managing elevated intracranial pressure (ICP), and addressing other neurologic and medical complications.

Triage

Prehospital management of acute ICH prioritizes airway maintenance, cardiovascular support, and rapid transport to the nearest acute stroke care facility [9].

ABCD Approach

  1. Airway: Assess airway patency. Intubation should only be performed if the patient cannot protect their airway or is in respiratory distress.
  2. Breathing: Ensure adequate oxygenation by administering supplementary oxygen if the patient is hypoxic, aiming to maintain oxygen saturation above 94%. Avoid hypoventilation, as increased partial pressure of carbon dioxide can cause cerebral vasodilation and elevate ICP.
  3. Circulation: Evaluate hydration status. All suspected ICH patients should initially be placed nil by mouth and started on IV isotonic saline to maintain serum sodium levels above 135 mmol/L. Hypotension should be promptly treated with fluid replacement. Elevated blood pressure must be carefully managed to avoid further complications.
  4. Disability: Assess the patient’s level of consciousness using the Glasgow Coma Scale (GCS). Conduct hourly neurologic evaluations to monitor for signs of deterioration or elevated ICP.

General Measures

  • Head Elevation: Elevate the head of the bed to greater than 30 degrees to promote venous drainage and reduce ICP [10].
  • Sedation: For intubated patients, use appropriate sedation, such as midazolam, to ensure patient comfort.
  • Temperature Control: Administer antipyretics, such as paracetamol, for temperatures above 38°C.
  • Head Positioning: Maintain a neutral head position, avoiding neck rotation or placing IV lines at the neck to prevent venous outflow obstruction.

Pharmacological Approach to Intracerebral Hemorrhage (Mnemonic: BCGO)

B: Blood Pressure Control
Blood pressure management is critical in ICH. The target systolic blood pressure (SBP) should be maintained between 140-160 mmHg, ideally achieved within the first hour of presentation using intravenous antihypertensive medications [11].

C: Coagulopathy Management
All anticoagulants and antiplatelet agents should be discontinued, and reversal agents should be administered when necessary [12, 13]. Platelet transfusion generally has a limited role. Examples of anticoagulants and their reversal strategies include:

  • Warfarin: Reversal with Vitamin K, fresh frozen plasma (FFP), or 4-factor Prothrombin Complex Concentrates (PCC), as it inhibits Vitamin K-dependent clotting factors (II, VII, IX, X).
  • Unfractionated Heparin: Reversal with Protamine, as it binds to antithrombin III.
  • Low Molecular Weight Heparin: Reversal is incomplete with Protamine, as it inhibits factor Xa.
  • Dabigatran: Reversal with Idarucizumab (Praxbind), which directly binds and inhibits thrombin (Factor IIa).
  • Oral Factor Xa Inhibitors (e.g., Apixaban (Eliquis), Edoxaban (Lixiana, Savaysa), Rivaroxaban (Xarelto)): Reversal options include Andexanet alfa (AndexXa) or 4-factor PCC.

G: Glucose Management
Blood glucose levels should be maintained within the range of 6-10 mmol/L to prevent hypoglycemia or hyperglycemia, both of which can exacerbate neurologic injury [14].

O: Osmotic Therapy
For patients with acute ICP elevation or life-threatening mass effect, treatment with mannitol or hypertonic saline may be considered. However, these therapies have not been shown to significantly improve outcomes in patients with acute ICH [15].

Patients with acute ICH are at risk for early seizures (within one to two weeks of ICH) and late (post-stroke) seizures. Early seizures may be self-limited, attributed to transient neurochemical changes associated with the acute ICH. For patients who have a seizure, immediate intravenous anti-seizure medication treatment should be initiated to reduce the risk of a recurrent seizure although anti-seizure treatments’ value is not clear [16].

Medications

Labetalol (Antihypertensive Medication)

  • Dose: (0.25-0.5 mg/kg). Initial bolus of 20 mg IV, followed by 20–80 mg IV bolus every 10 minutes (maximum total dose of 300 mg). Alternatively, 0.5 to 2 mg/minute can be administered as an IV loading infusion following an initial 20 mg IV bolus (maximum total dose of 300 mg).
  • Frequency: Administered every 10 minutes as required or as an infusion.
  • Maximum Dose: 300 mg total.
  • Cautions/Comments:
    • Always inquire about food or drug allergies, a past medical history of bronchial asthma, or heart failure.
    • Labetalol is classified as Category C in pregnancy for all trimesters.

Nicardipine (Antihypertensive Medication)

  • Dose: 5 to 15 mg/hour as IV infusion. Once the desired blood pressure is achieved, reduce the dose to a maintenance rate of 2–4 mg/hour.
  • Frequency: Continuous infusion.
  • Maximum Dose: 15 mg/hour.
  • Cautions/Comments:
    • Avoid use in patients with acute heart failure.
    • Use with caution in patients with coronary ischemia.
    •  

Phenytoin (Anti-Seizure Medication)

  • Dose: 15–20 mg/kg as a loading dose.
  • Frequency: Administered every 8 hours.
  • Maximum Dose: 100 mg.
  • Cautions/Comments:
    • Always check for food or drug allergies and any history of heart problems.
    • Phenytoin is classified as Category D in pregnancy for all trimesters.

Mannitol (For Treating High ICP – Osmotic Diuresis)

  • Dose: 2–4 ml/kg (12.5%), 1.25–2.5 ml/kg (20%), or 1–2 ml/kg (25%).
  • Frequency: Administer every 2 hours as required.
  • Cautions/Comments:
    • Ask about food or drug allergies.
    • Mannitol is classified as Category C in pregnancy for all trimesters.

Surgery

The surgical approach to managing intracerebral hemorrhage (ICH) often includes decompressive hemicraniectomy for hematoma evacuation. Immediate neurosurgical consultation is critical when imaging findings suggest the need for emergency surgery. Indications for urgent surgical intervention include cerebellar ICH that is either ≥3 cm³ in diameter or causing brainstem compression, intraventricular hemorrhage (IVH) with obstructive hydrocephalus and neurologic deterioration, and hemispheric ICH associated with life-threatening brain compression or obstructive hydrocephalus. These conditions demand prompt action to prevent further neurologic compromise and improve patient outcomes.

  •  

Special Patient Groups

Pediatrics

ICH in children is predominantly traumatic in origin, often resulting from head injuries caused by falls, vehicular accidents, or abuse (e.g., non-accidental trauma). Non-traumatic causes are less common but may include vascular anomalies like arteriovenous malformations, coagulopathies, or rare genetic conditions [17].

Geriatrics

The incidence of spontaneous ICH increases significantly with age, primarily due to the widespread use of anticoagulation and antithrombotic therapies for managing cardiovascular and cerebrovascular conditions [18]. In addition, older adults often have underlying medical conditions, such as hypertension, diabetes mellitus, and hypercholesterolemia, which predispose them to vascular fragility and hemorrhage. Careful monitoring and tailored management are required to address both the hemorrhage and these comorbidities in elderly patients.

Pregnant Patients

The risk of spontaneous ICH is elevated in pregnant women, especially in those with preeclampsia, eclampsia, or pregnancy-induced hypertension (PIH) [19]. These conditions are associated with endothelial dysfunction, elevated blood pressure, and increased risk of vascular rupture. Management in pregnant women involves a multidisciplinary approach, balancing maternal and fetal safety, with attention to blood pressure control and timely delivery if necessary.

When To Admit This Patient

All patients with ICH should be admitted to the intensive care unit (ICU) for comprehensive management [20]. ICU admission is crucial for close monitoring and intervention due to the potential for rapid deterioration in neurological status and the need for specialized care. These patients require the involvement of a multidisciplinary team, including neurosurgeons, neurologists, and critical care specialists, to address various aspects of care.

Key reasons for ICU admission include:

  1. Further Investigation: Advanced imaging, such as CT angiography or MRI, is often necessary to identify the underlying cause of the hemorrhage (e.g., aneurysm, arteriovenous malformation) and to assess for complications like hydrocephalus or increased intracranial pressure.
  2. Medical Management: Tight control of blood pressure, intracranial pressure, glucose levels, and coagulopathy is essential to prevent secondary brain injury and improve outcomes.
  3. Surgical Operations: Patients may require urgent surgical interventions, such as hematoma evacuation, decompressive craniectomy, or ventriculostomy, particularly in cases of life-threatening mass effect, brainstem compression, or obstructive hydrocephalus.
  4. Rehabilitation Planning: Early rehabilitation interventions should be initiated to minimize long-term disability. This includes physical therapy, occupational therapy, and addressing the patient’s psychological and cognitive needs post-ICH.

The ICU provides an ideal setting for continuous monitoring of neurological function, management of complications, and rapid response to emergencies such as rebleeding or sudden increases in intracranial pressure. Admission ensures a holistic and systematic approach to optimizing patient outcomes following spontaneous ICH.

Revisiting Your Patient

An urgent head CT was completed and revealed an intracranial hemorrhage in the caudate region.

During her ED stay, her GCS suddenly reduced to 7/15 (E2, V2, M3). She was intubated for airway protection. A repeated head CT demonstrated expansion of the right intracranial hemorrhage with intraventricular extension midline shift.

Intracranial Hemorrhage in the Caudate Region. An intracranial hemorrhage is visualized in the caudate region of the brain. Contributed by S Munakomi, MD [21]

The neurosurgical team was consulted, and the patient was sent for an emergency craniectomy and evacuation of the clot. A postoperative head CT showed a grossly evacuated blood clot and corrected midline shift. The intensive care team weaned her off of mechanical ventilatory support, and her GCS improved to 10 (E3, V1, M6).

Authors

Picture of Muhammad Izzat Abdul Hadi

Muhammad Izzat Abdul Hadi

Muhammad Izzat Bin Abdul Hadi is a dedicated emergency medicine professional at Hospital Universiti Sains Malaysia in Kelantan, Malaysia. He completed his medical degree at Mansoura University in 2007 and later obtained a Master of Medicine in Emergency Medicine from Universiti Sains Malaysia in 2019. His contributions to medical research include two notable publications in the Malaysian Journal of Emergency Medicine (M-JEM) in 2021.

Picture of Iskasymar Ismail

Iskasymar Ismail

Dr Iskasymar is an emergency physician, a senior medical lecturer at University Putra Malaysia (UPM) and Head of Unit of RESQ (Regional Emergency Stroke Quick Response) Stroke Emergency Unit in UPM teaching hospital, Hospital Sultan Abdul Aziz Shah (HSAAS). He is actively involved in making RESQ as niche service for hyperacute stroke care in HSAAS and working collectively with neurology team and radiology team in developing protocols and SOP. Dr Iskasymar is an active expert panel of stroke and intracranial hemorrhage Clinical Practice Guideline of Malaysia.

Picture of Kamarul Aryffin Baharuddin

Kamarul Aryffin Baharuddin

Dr. Kamarul Aryffin Baharuddin is a Professor in Emergency Medicine and an Emergency Medicine Specialist at the Universiti Sains Malaysia (USM), Kelantan, Malaysia. He graduated with his medical degree in 1998 and completed his postgraduate specialization in 2006. His research interests are neurological emergency, pain management, medical education, and artificial intelligence in medicine. He is currently a Deputy Dean of Academics in the School of Medical Sciences, USM. He is also one of the team in neurology SIG (Special Interest Group) under the College of Emergency Physician, Malaysia.

Picture of Erin Simon

Erin Simon

Dr. Erin L. Simon is a Professor of Emergency Medicine at Northeast Ohio Medical University. She is Vice Chair of Research for Cleveland Clinic Emergency Services and Medical Director for the Cleveland Clinic Bath emergency department. Dr. Simon serves as a reviewer for multiple academic emergency medicine journals.

Listen to the chapter

References

  1. Cheng Y lin.Molecular Mechanisms of Notch1-Mediated Neuronal Cell Death in Ischemic Stroke. PhD Thesis. The University of Queensland; 2014. doi:10.14264/uql.2014.547
  2. Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis – UpToDate. Accessed December 4, 2024. https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-pathogenesis-clinical-features-and-diagnosis
  3. Feigin VL, Brainin M, Norrving B, et al. World Stroke Organization (WSO): Global Stroke Fact Sheet 2022. Int J Stroke Off J Int Stroke Soc. 2022;17(1):18-29. doi:10.1177/17474930211065917
  4. Sheth KN. Spontaneous Intracerebral Hemorrhage. N Engl J Med. 2022;387(17):1589-1596. doi:10.1056/NEJMra2201449
  5. Pinnamaneni S, Aronow WS, Frishman WH. Neurocardiac Injury After Cerebral and Subarachnoid Hemorrhages. Cardiol Rev. 2017;25(2):89-95. doi:10.1097/CRD.0000000000000112
  6. Hemphill JC, Bonovich DC, Besmertis L, Manley GT, Johnston SC. The ICH score: a simple, reliable grading scale for intracerebral hemorrhage. Stroke. 2001;32(4):891-897. doi:10.1161/01.str.32.4.891
  7. Dusenbury W, Malkoff MD, Schellinger PD, et al. International beliefs and head positioning practices in patients with spontaneous hyperacute intracerebral hemorrhage. Ther Adv Neurol Disord. 2023;16:17562864231161162. doi:10.1177/17562864231161162
  8. Pandey AS, Xi G. Intracerebral hemorrhage: a multimodality approach to improving outcome. Transl Stroke Res. 2014;5(3):313-315. doi:10.1007/s12975-014-0344-z
  9. Gioia LC, Mendes GN, Poppe AY, Stapf C. Advances in Prehospital Management of Intracerebral Hemorrhage. Cerebrovasc Dis. Published online March 7, 2024. doi:10.1159/000537998
  10. Simmons BJ. Management of intracranial hemodynamics in the adult: a research analysis of head positioning and recommendations for clinical practice and future research. J Neurosci Nurs. 1997;29(1):44-49. doi:10.1097/01376517-199702000-00007
  11. Sato S, Carcel C, Anderson CS. Blood Pressure Management After Intracerebral Hemorrhage. Curr Treat Options Neurol. 2015;17(12):49. doi:10.1007/s11940-015-0382-1
  12. Grzegorski T, Andrzejewska N, Kaźmierski R. Reversal of antithrombotic treatment in intracranial hemorrhage–A review of current strategies and guidelines. Neurol Neurochir Pol. 2015;49(4):278-289. doi:10.1016/j.pjnns.2015.06.003
  13. Campbell PG, Sen A, Yadla S, Jabbour P, Jallo J. Emergency reversal of antiplatelet agents in patients presenting with an intracranial hemorrhage: a clinical review. World Neurosurg. 2010;74(2-3):279-285. doi:10.1016/j.wneu.2010.05.030
  14. Godoy DA, Piñero GR, Svampa S, Papa F, Di Napoli M. Hyperglycemia and short-term outcome in patients with spontaneous intracerebral hemorrhage. Neurocrit Care. 2008;9(2):217-229. doi:10.1007/s12028-008-9063-1
  15. Qureshi AI, Wilson DA, Traystman RJ. Treatment of elevated intracranial pressure in experimental intracerebral hemorrhage: comparison between mannitol and hypertonic saline. Neurosurgery. 1999;44(5):1055-1064. doi:10.1097/00006123-199905000-00064
  16. Gilad R, Boaz M, Dabby R, Sadeh M, Lampl Y. Are post intracerebral hemorrhage seizures prevented by anti-epileptic treatment?. Epilepsy Res. 2011;95(3):227-231. doi:10.1016/j.eplepsyres.2011.04.002
  17. Kumar R, Shukla D, Mahapatra AK. Spontaneous intracranial hemorrhage in children. Pediatr Neurosurg. 2009;45(1):37-45. doi:10.1159/000202622
  18. Berhouma M, Jacquesson T, Jouanneau E. Spontaneous Intracerebral Hemorrhage in the Elderly. Brain and Spine Surgery in the Elderly. 2017:411-22.
  19. Berhouma M, Jacquesson T, Jouanneau E. Spontaneous Intracerebral Hemorrhage in the Elderly. Brain and Spine Surgery in the Elderly. 2017:411-22.
  20. Goldstein JN, Gilson AJ. Critical care management of acute intracerebral hemorrhage. Curr Treat Options Neurol. 2011;13(2):204-216. doi:10.1007/s11940-010-0109-2
  21. Tenny S, Thorell W. Intracranial Hemorrhage. In: StatPearls. StatPearls Publishing; 2024. Accessed December 4, 2024. http://www.ncbi.nlm.nih.gov/books/NBK470242/

Reviewed and Edited By

Picture of Erin Simon, DO

Erin Simon, DO

Dr. Erin L. Simon is a Professor of Emergency Medicine at Northeast Ohio Medical University. She is Vice Chair of Research for Cleveland Clinic Emergency Services and Medical Director for the Cleveland Clinic Bath emergency department. Dr. Simon serves as a reviewer for multiple academic emergency medicine journals.

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 Ischemic Stroke (2024)

~ iEM Education Project Team ~ Leave a comment

by Hassan Khuram, Parker Maddox, & Scott Goldstein

Authors
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You have a new patient!

Mrs. A, a 63-year-old female, was brought to the emergency department by her daughter after she noticed that her mother was unable to speak normally, and her face was droopy on the right side. Upon arrival, Mrs. A was lying on a stretcher in no acute distress. The daughter reported that her symptoms started suddenly about 30 minutes ago. 

The image was produced by using ideogram 2.0

Vital signs showed a blood pressure of 170/90 mmHg, heart rate of 90 beats per minute, respiratory rate of 18 breaths per minute,  Temperature is 36.6 C (98 F), and oxygen saturation of 98% on room air. The patient had a history of hypertension, hyperlipidemia, and type 2 diabetes mellitus. On neurological examination, Ms. A was found to have right-sided facial droop, right arm pronator drift, and slurred speech. The NIH Stroke Scale (NIHSS) score was 8.

What do you need to know?

Importance

Acute ischemic stroke (AIS) is a major public health concern that affects millions of people worldwide. Stroke, ischemic or hemorrhagic, is the third most common cause of disability and the second most common cause of death worldwide [1]. It is estimated that 12.2 million strokes occur around the world annually, with the vast majority being ischemic [1,2]. Early recognition and management of acute ischemic stroke are vital as outcomes are directly tied to the time between the onset of symptoms and initiation of treatment. For every hour treatment is delayed, the brain loses as many neurons as it does in approximately 3.6 years of normal aging, which has led to the adage “time is brain” [3]. Therefore, emergency department physicians must be well-versed in diagnosing and managing acute ischemic stroke to maximize patient outcomes. The main goals in the acute management of ischemic stroke are to minimize ischemic damage to the penumbra, treat any complications because of the infarction, and diagnose the etiology to prevent a recurrence. The primary objectives of this chapter are to present a thorough overview of the major ideas and practices involved in the early evaluation and treatment of acute ischemic stroke in the emergency room.

Epidemiology

Understanding epidemiology can help elucidate risk factors that can result in faster recognition of stroke and its acute management. The vast majority of strokes occur beyond the 5th decade, with the age of onset being lower in low to middle-income countries [4]. In an acute setting, it is critical to identify if a stroke is ischemic or hemorrhagic, as treatment varies significantly [4,11]. This risk increases significantly with age, along with other lifestyle factors. These factors are listed in the table below (with the highest risk factors listed in descending order.)

Table 1. Modifiable and Non-modifiable risk factors for stroke [1,4–6]

Modifiable Risk Factors

Non-Modifiable Risk factors

Hypertension

Prior history of stroke or TIA

Cigarette smoking

Age ≥ 65 years

Diabetes mellitus

Sex ♂ > ♀

Atrial Fibrillation

Family History

Carotid artery stenosis

Genetic disorders (e.g., sickle cell)

Dyslipidaemia

Migraine with aura

Obesity and Metabolic syndrome

 

Diet/Nutrition

 

Sedentary Behavior

 

Alcohol/Recreational drug use (e.g. cocaine) 

 

Coagulopathy

 

Hormone Replacement Therapy/OCP

 

Pathophysiology

Acute ischemic strokes can occur due to thrombotic or embolic causes. One common link behind all the risk factors discussed above is that, in one form or another, they cause damage or dysfunction to blood vessels in the brain, reducing blood flow to the brain. Consequently, the parenchyma of the brain is unable to carry out its metabolic functions, which eventually leads to necrosis [7]. The exact mechanisms of how different risk factors contribute to stroke vary, but they ultimately all result in the damage of blood vessels in the brain. While there are many causes behind the damage of blood vessel walls, atherosclerosis and Virchow’s triad- blood stasis, endothelial injury, and hypercoagulability- remain the primary pathological process behind the vast majority of strokes [6,7]. For example, in Hypertension, the high pressures in the vessels cause shearing of the endothelial lining of blood vessel walls, which can result in rupture or thrombus formation. As the atherosclerotic plaques grow and become more advanced, they can lead to blood flow obstruction and turbulence, which can promote blood stasis. Blood stasis, in turn, can increase the risk of thrombosis within the affected blood vessel. The formation of a thrombus can obstruct blood flow to the brain and cause a stroke [7].

Similarly, smoking can cause inflammation and oxidative stress on blood vessels, causing an inflammatory response that ultimately results in the narrowing of the vessels and thrombus formation [8]. This framework also explains why older individuals are at higher risk since they have an increased prevalence of the modifiable risk factors listed in Table 1. [9]. Etiologies arising from circulatory system issues outside the brain require additional urgent management [5].

Medical History

A good history remains a key cornerstone in evaluating and managing stroke patients. Most typical presentations of strokes will be older adults presenting with acute onset focal neurological deficits. Patients might present with complaints of sudden onset speech difficulties, vision, sensation, strength, or coordination [10]. The acuity of neurologic dysfunction should clue physicians that stroke is an important differential. Another vital component when suspecting stroke is determining the time since the onset of symptoms. If this is unknown, then the last time the patient was seen well or at their neurological baseline can be used as a surrogate [11]. This step is critical as it helps determine whether the patient is within the window for reperfusion therapy and endovascular thrombectomy [5]. The 6S mnemonic list in Table 2. can be utilized to help clue clinicians that the patient might be having a stroke [12]:

Table 2. 6S mnemonic detailing core signs of stroke

S

Sudden onset

S

Slurred speech

S

Side weakness (unilateral deficits in face, arm, or leg)

S

Spinning (Vertigo)

S

Severe headache

S

Seconds (time since symptoms started)

The presence of this constellation should cue physicians to the immediate need for further evaluation of a serious process requiring labs and neuroimaging. The collection of symptoms can also give clues as to which vascular territory might be affected and can prompt the clinician to evaluate for further signs in that territory to help confirm the location. A general gestalt listed in Table 3. below can be used to help clinicians orient themselves as to which general vascular territory in the brain might be affected and what questions/exam findings to further probe for. The table is not exhaustive or mutually exclusive, and a more detailed discussion of the lesion site and associated neurologic findings is presented in the physical exam section.

Table 3. List of deficits and their associated territories [13]

Vascular territory

Associated deficits

Anterior Cerebral Artery (ACA)

Feet and legs

Middle Cerebral Artery (MCA)

Hands, Arms, Face, and Speech

Posterior Cerebral Artery (PCA)

Visual

Vertebrobasilar Artery (Brainstem)

Crossed signs (Contralateral hemiplegia & ipsilateral cranial nerve abnormalities)

Cerebellar Arteries

Coordination

The pace and course of symptoms can clue clinicians into the different subtypes of stroke that may be affecting the patient. Acute ischemic strokes due to embolic sources tend to occur suddenly, and the maximal deficit is perceived during this time. However, etiologies due to thrombosis tend to fluctuate and progress stepwise [14].

Other crucial components of medical history to assess are the risk factors mentioned in Table 1. They can help determine the precipitating factor for the stroke and can help guide management. For example, if the patient has a history of atrial fibrillation or carotid artery stenosis, then that could explain an embolic cause for the stroke and would require a more extensive workup along with additional management measures. Hypertension should also be sought out as it is the number one modifiable risk factor for stroke [2,6]. A review of current medications is also important because it can affect management. If a patient has been on anti-coagulation medications, then that is a strict contraindication for thrombolytics in stroke as it may lead to a hemorrhagic conversion [15]. In patients with acute ischemic stroke, a detailed medical history is crucial in directing the diagnostic and therapeutic decision-making process.

Physical Examination

Based on history, a focused physical and neurological exam can aid in localizing the lesion and provide clues as to the cause. Time is brain, and therefore, clinical suspicion of acute ischemic stroke should be rapidly confirmed with physical exam findings to minimize the time between the door to neuroimaging and recognize candidates for reperfusion therapy or endovascular thrombectomy [5,11,15]. As in all emergent cases, airway, breathing, circulation, disability, and exposure (ABCDE) should be prioritized in that order before attending to other steps in management. The physical exam should be tailored based on history to save time.

For example, if there is a history of atrial fibrillation, then a cardiac exam should be conducted to look for murmurs that might indicate an embolic cause. Patients with a history of atherosclerosis risk factors should also be examined for bruits in the neck that may reveal an embolic source. Papilledema on ocular exam may signify possible hemorrhagic stroke or cerebral edema as a complication of stroke that requires immediate intervention [16]. A neurologic exam is vital to confirm clinical suspicion of stroke and rule out other stroke mimics such as hypoglycemia or Bell’s palsy. Deficits on the exam can help point the clinician to the location of the lesion and the severity of the prognosis [13]. Table 4 below can be used to help localize the lesion based on clinical symptoms.

Table 4. A non-exhaustive list of common brain lesions and associated symptoms [13]

Vascular Territory

Common Neurologic Findings

Anterior Cerebral Artery (ACA)

  • Contralateral somatosensory & motor deficit mostly in lower extremity
  • Abulia
  • Urinary incontinence
  • Emotional disturbance

Middle Cerebral Artery (MCA)

  • Aphasia (dominant hemisphere)
  • Hemineglect (non-dominant hemisphere)
  • Contralateral somatosensory & motor deficit mostly in upper limbs and lower half of face than lower limbs
  • Conjugate eye deviation towards side of infract
  • Contralateral homonymous hemianopia without macular sparing

Posterior Cerebral Artery (PCA)

  • Agnosia and alexia without agraphia (Dominant hemisphere)
  • Prosopagnosia (Non-dominant hemisphere)
  • Contralateral homonymous hemianopia with macular sparing

Anterior inferior cerebellar artery (AICA)

  • Ipsilateral deafness, facial motor/sensory loss, limb ataxia
  • Decreased pain/temperature in contralateral body

Posterior inferior cerebellar artery (PICA)

  • Ipsilateral palatal weakness, limb ataxia
  • Wallenberg syndrome
  • Decreased pain/temperature in contralateral body

Vertebrobasilar system lesion (brainstem)

  • Contralateral hemiplegia & ipsilateral cranial nerve abnormalities (Crossed signs)
  • Possible ataxia

The National Institutes of Health Stroke Scale (NIHSS) is one of the most studied and validated scales in clinical practice that should be used to provide a structured and quantifiable neurologic examination [5,11,12,16]. It includes 11 items (Table 5) and can be done in less than 10 minutes. The scale can quantify neurologic deficits and provide information about patient outcomes [17]. Facial paresis, arm weakness, and abnormal speech on the NIHSS are the most predictive findings for acute ischemic stroke [18].

Table 5. Snapshot of the National Institute of Health Stroke Scale (NIHSS) [5,19]

Instructions

Scale Definition

1a. Level of consciousness (LOC) 

0 = Alert

1 = Drowsy- arousable by minor stimulation to obey, answer, or respond

2 = Obtunded; requires repeated stimulation to attend or is obtunded and requires strong or painful stimulation to make movements (not stereotyped).

3 = Unresponsive; Responds only with reflex motor or autonomic effects or unresponsive, flaccid, and areflexic.

1b. Orientation Questions (2)

0 = Answers both questions correctly.

1 = Answers one question correctly.

2 = Answers neither question correctly.

1c. Response to commands (2)

0 = Performs both tasks correctly

1 = Performs 1 task correctly

2 = Performs neither

2. Gaze

0 = Normal horizontal movements

1 = Partial gaze palsy

2 = Complete gaze palsy

3. Visual fields

0 = No visual field defect

1 = Partial hemianopia

2 = Complete hemianopia

3= Bilateral hemianopia

4. Facial movement

0 = Normal

1 = Minor facial weakness

2 = Partial facial weakness

3= Complete unilateral palsy

5. Motor function (Arm)

5a. Left arm

5b. Right arm

 

0 = No drift

1 = Drift before 10 s

2 = Falls before 10 s

3= No effort against gravity

4=No movement

6. Motor function (Leg)

6a. Left leg

6b. Right leg

 

0 = No drift

1 = Drift before 10 s

2 = Falls before 10 s

3= No effort against gravity

4=No movement

7. Limb ataxia

0 = No ataxia

1 = Ataxia in 1 limb

2 = Ataxia in 2 limbs

3= No effort against gravity

4=No movement

8. Sensory

0 = No sensory loss

1 = Mild sensory loss

2 = Severe sensory loss

9. Language

0 = Normal

1 = Mild aphasia

2 = Severe aphasia

3= Mute or global aphasia

10. Articulation

0 = Normal

1 = Mild dysarthria

2 = Severe dysarthria

11. Extinction or inattention

0 = Absent

1 = Mild loss (1 sensory modality lost)

2 = Severe loss (2 modalities lost)

Vital signs play a critical role in the evaluation and management of acute ischemic stroke and conditions that may mimic stroke. Temperature, in particular, is a key parameter, as abnormalities can influence neurological function and mimic or exacerbate stroke symptoms. Hyperthermia (elevated body temperature) is associated with worsened outcomes in stroke patients due to increased metabolic demand and potential exacerbation of ischemic injury. On the other hand, hypothermia (lowered body temperature) can also cause altered mental status, which may resemble stroke-like presentations. Monitoring and correcting these temperature abnormalities is essential to optimize neurological recovery and rule out underlying infections or systemic conditions. Additionally, blood pressure, heart rate, respiratory rate, and oxygen saturation must be carefully assessed, as significant deviations can indicate complications such as increased intracranial pressure, arrhythmias, or hypoxia, which can impact stroke presentation and management.

Alternative Diagnoses

The differential diagnosis for acute-onset focal neurologic deficits, such as those found in acute ischemic stroke, is broad, and it is important to have a framework to rule out other causes. The VIINDICATES mnemonic (Table 6) can be useful in grouping the most frequent and important causes of acute neurologic dysfunction [20].

Table 6. Non-exhaustive differential diagnosis of acute ischemic stroke [21]

Vascular

Hemorrhagic stroke, cerebral venous thrombosis, arteriovenous fistulas, aneurysms

Infectious

Meningitis, Encephalitis, Progressive multifocal leukoencephalopathy

Immune system dysfunction/autoimmune

Multiple Sclerosis, Bell palsy, Guillain-Barré syndrome, Anti-NMDA encephalitis

Neoplasm

Brain tumors, paraneoplastic syndromes, lung cancer

Drugs

Alcohol withdrawal, drug intoxication (opioids, barbiturates, etc.)

Cerebral/Neurologic

Transient ischemic attack (TIA), syncope, seizure, postictal paralysis, migraine aura

Trauma

Traumatic brain injury, Subdural hematoma, epidural hematoma, Brown-Séquard syndrome

Endocrine/Metabolic

Diabetic Ketoacidosis, hyponatremia, hypoglycemia

Social/Psychiatric

Conversion disorder, malingering

The clinician must pay close attention to the physical exam and medical history results that may favor one of these diagnoses over another to distinguish between them. Timing is critical and it is important to understand if the symptoms appeared suddenly or have been slowly brewing over time [12,16,21].

Acing Diagnostic Testing

When suspicion of acute ischemic stroke is high, time is of the essence due to the time limitations of thrombolytics or mechanical thrombectomy. Therefore, oxygen saturation, finger stick blood glucose, non-contrast head CT and angiography should be prioritized over all other tests as they are the only requirements before the administration of thrombolytics [5,11]. Oxygen saturation can help rule out hypoxia as a cause of neurological dysfunction [12,21]. Blood glucose is important as it can rule out hypoglycemia, DKA, or hyperosmolar hyperglycaemic state, which can all present like symptoms of stroke and can worsen outcomes with the administration of thrombolytics [22]. Neuroimaging is essential because it can help differentiate acute ischemic stroke from a hemorrhagic stroke, which has very different management. Neuroimaging can also rule out most other differential diagnoses discussed earlier when combined with physical history and exam. Loss of grey-white differentiation is an early CT finding in ischemic stroke, while increased density within the occluded vessel can represent a thrombus (Figure 1) [5,13,15,16,23].

Figure 1 - Non-contrast computed tomography (CT) with multiple planar reconstructions (MPR) revealed a hyperdense middle cerebral artery (MCA) sign in the left MCA (Picture A and B, arrow). Repeat CT after completion of the alteplase administration revealed resolution of the hyperdense MCA sign but the appearance of an M2 dot sign (Picture C and D, arrowhead). Angiography showed the occlusion of the left MCA M2 segment, corresponding to the M2 dot sign (Picture E, arrowhead) [23].jpg

Complete blood counts and coagulation studies should not delay the administration of thrombolytic therapy unless there is a high suspicion of coagulopathy or a history of the patient being on anticoagulating agents [5,12,16].

Electrocardiogram and cardiac markers such as troponin are also important to rule out cardiac causes. They may illuminate a source for emboli, such as atrial fibrillation, but this should not delay neuroimaging [5].

Other non-urgent lab tests that may be indicated depending on patient presentation include [5,10]:

Complete Metabolic Panel (CMP): Assesses electrolyte imbalances, renal function, and glucose levels, which are critical in stroke patients to rule out mimicking conditions (e.g., hypoglycemia) and to ensure safe administration of interventions like thrombolysis.

Blood Alcohol Level and Toxicology Screen: Helps identify substances that might contribute to altered mental status or stroke-like symptoms, such as intoxication or drug use, which can influence treatment decisions and prognosis.

Pregnancy Test in Women of Childbearing Age: Mandatory before imaging procedures involving radiation (e.g., CT) or medications (e.g., thrombolytics), as these might pose risks to a fetus.

Arterial Blood Gas (ABG): Assesses oxygenation, ventilation, and acid-base status. Useful in patients with suspected respiratory compromise or to evaluate hypoxia, which may exacerbate neurological deficits.

Chest Radiograph (CXR): Evaluates for underlying or concurrent conditions such as pneumonia, aspiration, or cardiac issues (e.g., heart failure) that could complicate stroke management.

Lumbar Puncture (LP): Performed if a hemorrhage is strongly suspected but not visible on a CT scan. Helps detect xanthochromia or elevated red blood cell count, which are indicative of subarachnoid hemorrhage.

Electroencephalogram (EEG): Recommended if seizures are suspected, as post-stroke seizures or seizure-like activity can mimic stroke symptoms or complicate recovery.

Urinalysis and Blood Cultures: Indicated in febrile patients to identify infections, such as urinary tract infections or sepsis, which might cause or exacerbate stroke-like presentations and impact recovery.

Blood Type and Cross-Match: Necessary if there is coagulopathy requiring reversal with fresh frozen plasma or if massive blood transfusion is anticipated in cases of hemorrhagic transformation.

MRI: Provides superior imaging of the brain compared to CT, identifying small or early infarcts and areas of ischemia. MRI is particularly valuable for stroke patients with ambiguous CT findings.

Risk Stratification

The presence of certain red flags, such as severe headache, papilledema, neck stiffness, loss of consciousness, or rapidly worsening neurological deficits, may indicate a worse outcome and the need for more aggressive management. These symptoms may indicate that the lesion has affected certain vital regions in the brain or there has been a conversion to hemorrhagic stroke [5,11]. Severe hypo/hyperglycemia (glucose < 50 mg/dL or > 400 mg/dL) or hypertension (> 185/110 mm Hg) also indicate a poor outcome as these need to be managed before reperfusion therapy can be utilized, which results in further neurologic insult [5]. The NIHSS score can be utilized to predict outcomes such as disability, recurrent stroke, or death. The higher the NIHSS score, the more severe the stroke and the worse the prognosis. In general, patients with an NIHSS score of 0-4 have a good prognosis, while those with a score of 20 or higher have a higher risk of death or severe disability [5,17,24].

Management

Stroke patients are treated as critically ill patients and require urgent management. This includes assessing and stabilizing the patient’s airway, breathing, and circulation (ABCs), conducting a thorough evaluation to determine whether thrombolytic therapy is appropriate, and addressing any underlying medical conditions, such as hypertension, that may complicate treatment [5,12,16].

Airway and breathing can be compromised due to damage to areas central to consciousness, breathing, or swallowing as listed in Table 7.

Table 7. Possible locations of lesions compromising the airway [25]

Levels of Consciousness

Breathing

Swallowing

Thalami

respiratory centers in the cortex, pons, and medulla

Medulla & brainstem connections

Limbic system

Pons

 

Reticular formation in the brainstem

Medulla

 

Damage to any of these areas requires securing the airway and maintaining breathing by positing the head of the bed to 30° to prevent aspiration. The specific approach will depend on the severity of the patient’s presentation [25].  Assessing the level of consciousness can provide valuable information to guide judgment. If a patient is awake, alert, and responsive, then they may be able to secure their airway and provide adequate ventilation on their own. Respiratory rate and effort should be assessed by looking for the rate of breathing, use of accessory muscles, or increased work of breathing. Airway patency can be determined by looking for signs of obstruction, such as snoring or stridor [16]. If oxygen saturation is below 94%, supplemental oxygen should be provided. Oxygen support is not beneficial if saturation is above 94% [5]. It is important to note that the neurologic exam can be severely limited if the patient requires intubation. Therefore, the clinician should pick up on subtle signs since the interaction with the patient began that can clue the physician on the baseline status, such as language function or any asymmetric motor activity, before the patient is pharmacologically paralyzed to be intubated [10].

 

Once breathing is secured, the next step is to ensure circulation is not compromised. Patients presenting with acute ischemic stroke frequently will be hypertensive as this is the body’s natural response to reperfuse the ischemic regions [16]. However, it is also not uncommon for patients to present with hypotension and hypovolemia. Due to the time-sensitive nature of acute ischemic stroke, correcting blood pressure takes priority [5]. When a patient with acute ischemic stroke has severe hypertension (systolic blood pressure >220 mmHg or diastolic blood pressure >120 mmHg), it may be necessary to lower their blood pressure to a safe level as administration of thrombolytics at this level can lead to hemorrhage [15]. Medications such as intravenous labetalol, nicardipine, or clevidipine can be used for cautious reduction (Table 8).

Table 8. Drug dosing for treatment of arterial hypertension in acute ischemic stroke [5]

Labetalol

10–20 mg IV over 1–2 min, may repeat 1 time

Nicardipine

5 mg/h IV, titrate up by 2.5 mg/h every 5–15 min, maximum 15 mg/h; when desired BP reached, adjust to maintain proper BP limits

Clevidipine

1–2 mg/h IV, titrate by doubling the dose every 2–5 min until desired BP reached; maximum 21 mg/h

In randomized controlled trials (RCTs) of intravenous (IV) thrombolytics, patients were required to have a systolic blood pressure <185 mm Hg and a diastolic blood pressure <110 mm Hg before treatment and <180/105 mm Hg for the first 24 hours after treatment [5]. Therefore, it is reasonable to aim for the blood pressure targets used in the RCTs of IV alteplase. In contrast, for patients with mild to moderate hypertension, it is generally advised to withhold blood pressure-lowering medications in the first few hours after the onset of stroke. This is because the rapid reduction in blood pressure can decrease cerebral perfusion and worsen ischemic injury [7].

Following stabilization, neuroimaging and lab tests discussed in the diagnostic test are prioritized to further aid in management. Figure 2 summarizes the steps discussed so far.

Figure 2 - Initial Management of Stroke

Once the diagnosis of acute ischemic stroke has been established, the next step is to figure out if the patient is eligible for thrombolysis (Table 9).

Table 9. Inclusion and exclusion criteria for rtTPA [5,15]

Inclusion Criteria

  • patients ≥ 18 years old
  • symptom onset within 4.5 hours
  • meets clinical criteria e.g. ischemic stroke

Strict Exclusion Criteria

  • History of ischemic stroke, severe head trauma, intracranial surgery, and intracanal hemorrhage within the last 3 months
  • Blood pressure > 185/110 mm Hg
  • Platelets <100,000/mm3 or glucose <50 mg/dL
  • Anticoagulant use with INR > 1.7, PT >15 sec, or increase in active PTT
  • Active intracranial bleeding
  • Intracranial neoplasm

Intravenous recombinant tissue plasminogen activator (tPA) agents such as Alteplase or Tenecteplase should be used (Table 10) [5,15,26]. Mechanical thrombectomy may be indicated if a large artery occlusion (LVO) is causing a stroke, and it has been less than 24 hours since symptom onset. The eligibility for mechanical thrombectomy and thrombolysis in individuals with ischemic stroke is assessed separately.  Patients may be qualified for one, both, or neither of these treatments depending on the timing of their appearance (4.5 hours for thrombolysis, 24 hours for mechanical thrombectomy) [5,27]. However, if the patient is not eligible for either chemical thrombolysis or mechanical thrombectomy, immediate dual antiplatelet therapy (DAPT) with agents such as aspirin and clopidogrel should begin [5,28]. In the acute management of ischemic stroke (even if caused by atrial fibrillation [AF]), parenteral anticoagulation (e.g., intravenous heparin) should not be used because it increases the chance of hemorrhagic conversion [5,11].

Table 10. Dosing for rtTPA in the management of acute ischemic stroke [5]

Alteplase

IV 0.9 mg/kg over 60 minutes (max. dose 90 mg), with an initial 10% of dose given as a bolus over 1 minute

Tenecteplase

IV 0.25 mg/kg as a bolus, max. dose 25 mg

Aspirin

160 to 325 mg loading dose, followed by 50 to 100 mg daily (for 21 days)

Clopidogrel

300 to 600 mg loading dose, followed by 75 mg daily (for 21 days)

Special Patient Groups

When a patient presents with symptoms of acute ischemic stroke, clinical considerations differ based on age and special patient groups. Pediatric patients may experience stroke due to congenital heart disease, sickle cell disease, or infections. Symptoms may be less obvious and include seizures, vomiting, and headaches [29]. Diagnosis of stroke in pregnant patients is challenging, and thrombolytic agents may increase the risk of hemorrhage in both the mother and fetus [30]. Special patient groups, including those with sickle cell anemia or undergoing surgery, may also be at increased risk of stroke and require careful management. Treatment options should be carefully considered in these patient groups with an understanding of the potential risks and benefits [31].

When To Admit This Patient

Patients with acute ischemic stroke are generally admitted to the hospital for further investigations and treatment [5]. Early discharge may be considered for patients with mild symptoms, no significant comorbidities, and a low risk of complications, provided they have a reliable caregiver and access to appropriate follow-up care. Severe or progressive symptoms, significant comorbidities, or high risk of complications require admission to a stroke unit or critical care unit [5,16]. Discharge decisions should be based on a careful assessment of clinical status, risk of complications, and social circumstances. Clear instructions on medication, follow-up care, and stroke prevention strategies should be provided, along with safety-netting arrangements for timely and appropriate care if complications or worsening symptoms occur after discharge [5,32].

Revisiting Your Patient

Based on the initial assessment, Mrs. A is presenting with symptoms that are consistent with a stroke. The patient’s daughter reported that the symptoms started suddenly, and upon examination, Mrs. A has right-sided facial droop, right arm drift, and slurred speech. Her past medical history is significant for hypertension, hyperlipidemia, and type 2 diabetes mellitus. The NIHSS score of 8 indicates a moderate to severe stroke. Immediate management includes stabilizing the patient’s vital signs and providing supportive care, including oxygen and intravenous access. Given the suspicion of a stroke, a non-contrast head CT scan should be obtained to rule out a hemorrhagic stroke. Mrs. A should be considered for thrombolytic therapy with alteplase as she is within the appropriate time window, and there are no contraindications.

Authors

Picture of Hassan KHURAM BS, MS

Hassan KHURAM BS, MS

Hassan Khuram is a 4th year medical student at Drexel University College of Medicine, with a background in psychology, biotechnology, and business of healthcare. He graduated Magna Cum Laude with a Bachelor of Science in Psychology from Virginia Commonwealth University and a Master of Science in Biotechnology from Georgetown University. He is passionate about neurocritical care, medical education, and bioethics. He has an extensive background in research, having conducted studies on various subjects, including substance misuse, Parkinson's disease, mindfulness meditation and more. He has published articles on neurological emergencies and ethical issues in neurological care.

Picture of Parker MADDOX BA, MS

Parker MADDOX BA, MS

Parker Maddox is a fourth-year medical student at Sidney Kimmel Medical College at Thomas Jefferson University in Philadelphia. He graduated from the University of Virginia with a double major in Biology and Chemistry and went on to obtain a master’s degree in Biophysics and Physiology at Georgetown University. Since arriving to medical school, Parker has developed a passion for Emergency Medicine and has performed research on a wide range of topics including early sepsis recognition, pandemic viruses including Coronavirus 2019 and Monkeypox, ischemic stroke, Bell’s palsy, and international ECMO critical care protocol. This work has yielded multiple publications and a presentation at the Society for Academic Emergency Medicine (SAEM) 2022 Conference.

Picture of Scott GOLDSTEIN, DO, FACEP, FAEMS, FAAEM, EMT-PHP

Scott GOLDSTEIN, DO, FACEP, FAEMS, FAAEM, EMT-PHP

Dr. Scott Goldstein started his medical career at New York College of Osteopathic Medicine in New York where he received his Doctorate of Osteopathy and continued his training at Einstein Healthcare Network in the field of  Emergency Medicine, Philadelphia. Dr. Goldstein is dual-boarded through the American Board of Emergency Medicine in Emergency Medicine and Emergency Medicine Services (EMS). He currently works at a Level 1 academic trauma center, Temple University Hospital, in Philadelphia where he is the Chief of EMS and Disaster Medicine. He has continued to be an active member of the education community and EMS community where he holds the title of Fellow of American College of Emergency Medicine through ACEP, Fellow of the Academy of Emergency Medical Services through NAEMSP and Fellow of the American Academy of Emergency Medicine through AAEM.  His current academic title is one of Clinical Associate Professor of Emergency Medicine at Lewis Katz School of Medicine at Temple University. 

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References

  1. Feigin VL, Brainin M, Norrving B, et al. World Stroke Organization (WSO): Global Stroke Fact Sheet 2022. Int J Stroke. 2022;17(1):18-29. doi:10.1177/17474930211065917
  2. Heart Disease and Stroke Statistics—2022 Update: A Report From the American Heart Association | Circulation. Accessed March 27, 2023. https://www.ahajournals.org/doi/10.1161/CIR.0000000000001052
  3. Saver JL. Time Is Brain—Quantified. Stroke. 2006;37(1):263-266. doi:10.1161/01.STR.0000196957.55928.ab
  4. Saini V, Guada L, Yavagal DR. Global Epidemiology of Stroke and Access to Acute Ischemic Stroke Interventions. Neurology. 2021;97(20 Suppl 2):S6-S16. doi:10.1212/WNL.0000000000012781
  5. Powers WJ, Rabinstein AA, Ackerson T, et al. Guidelines for the Early Management of Patients With Acute Ischemic Stroke: 2019 Update to the 2018 Guidelines for the Early Management of Acute Ischemic Stroke: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association. Stroke. 2019;50(12). doi:10.1161/STR.0000000000000211
  6. Boehme AK, Esenwa C, Elkind MSV. Stroke Risk Factors, Genetics, and Prevention. Circ Res. 2017;120(3):472-495. doi:10.1161/CIRCRESAHA.116.308398
  7. Kuriakose D, Xiao Z. Pathophysiology and Treatment of Stroke: Present Status and Future Perspectives. Int J Mol Sci. 2020;21(20):7609. doi:10.3390/ijms21207609
  8. Ambrose JA, Barua RS. The pathophysiology of cigarette smoking and cardiovascular disease: an update. J Am Coll Cardiol. 2004;43(10):1731-1737. doi:10.1016/j.jacc.2003.12.047
  9. Head T, Daunert S, Goldschmidt-Clermont PJ. The Aging Risk and Atherosclerosis: A Fresh Look at Arterial Homeostasis. Front Genet. 2017;8:216. doi:10.3389/fgene.2017.00216
  10. Goldstein JN, Greer DM. Rapid focused neurological assessment in the emergency department and ICU. Emerg Med Clin North Am. 2009;27(1):1-16, vii. doi:10.1016/j.emc.2008.07.002
  11. Herpich F, Rincon F. Management of Acute Ischemic Stroke. Crit Care Med. 2020;48(11):1654-1663. doi:10.1097/CCM.0000000000004597
  12. Chugh C. Acute Ischemic Stroke: Management Approach. Indian J Crit Care Med Peer-Rev Off Publ Indian Soc Crit Care Med. 2019;23(Suppl 2):S140-S146. doi:10.5005/jp-journals-10071-23192
  13. Balami JS, Chen RL, Buchan AM. Stroke syndromes and clinical management. QJM Int J Med. 2013;106(7):607-615. doi:10.1093/qjmed/hct057
  14. Caplan LR, Gorelick PB, Hier DB. Race, sex and occlusive cerebrovascular disease: a review. Stroke. 1986;17(4):648-655. doi:10.1161/01.str.17.4.648
  15. Wardlaw JM, Murray V, Berge E, del Zoppo GJ. Thrombolysis for acute ischaemic stroke. Cochrane Database Syst Rev. 2014;2014(7):CD000213. doi:10.1002/14651858.CD000213.pub3
  16. Bevers MB, Kimberly WT. Critical Care Management of Acute Ischemic Stroke. Curr Treat Options Cardiovasc Med. 2017;19(6):41. doi:10.1007/s11936-017-0542-6
  17. Fonarow GC, Saver JL, Smith EE, et al. Relationship of national institutes of health stroke scale to 30-day mortality in medicare beneficiaries with acute ischemic stroke. J Am Heart Assoc. 2012;1(1):42-50. doi:10.1161/JAHA.111.000034
  18. Goldstein LB, Simel DL. Is this patient having a stroke? JAMA. 2005;293(19):2391-2402. doi:10.1001/jama.293.19.2391
  19. NINDS Know Stroke Campaign – NIH Stroke Scale. Accessed April 1, 2023. https://www.stroke.nih.gov/resources/scale.htm
  20. General Principles. UW Radiology. Accessed April 1, 2023. https://rad.washington.edu/about-us/academic-sections/musculoskeletal-radiology/teaching-materials/online-musculoskeletal-radiology-book/general-principles/
  21. Vilela P. Acute stroke differential diagnosis: Stroke mimics. Eur J Radiol. 2017;96:133-144. doi:10.1016/j.ejrad.2017.05.008
  22. Hafez S, Coucha M, Bruno A, Fagan SC, Ergul A. Hyperglycemia, Acute Ischemic Stroke and Thrombolytic Therapy. Transl Stroke Res. 2014;5(4):442-453. doi:10.1007/s12975-014-0336-z
  23. Ohno Y, Oomura M, Sakurai K, Matsukawa N. Hyperdense Vessel Signs Showing Migration of a Thrombus. Intern Med. 2017;56(4):465-466.
  24. Wityk RJ, Pessin MS, Kaplan RF, Caplan LR. Serial assessment of acute stroke using the NIH Stroke Scale. Stroke. 1994;25(2):362-365. doi:10.1161/01.str.25.2.362
  25. Bösel J. Use and Timing of Tracheostomy After Severe Stroke. Stroke. 2017;48(9):2638-2643. doi:10.1161/STROKEAHA.117.017794
  26. Evidence that Tenecteplase Is Noninferior to Alteplase for Acute Ischemic Stroke | Stroke. Accessed April 2, 2023. https://www.ahajournals.org/doi/10.1161/STROKEAHA.119.025080
  27. Jadhav AP, Desai SM, Jovin TG. Indications for Mechanical Thrombectomy for Acute Ischemic Stroke: Current Guidelines and Beyond. Neurology. 2021;97(20 Supplement 2):S126-S136. doi:10.1212/WNL.0000000000012801
  28. Antiplatelet Therapy in Ischemic Stroke and Transient Ischemic Attack | Stroke. Accessed April 2, 2023. https://www.ahajournals.org/doi/full/10.1161/STROKEAHA.118.023954
  29. Ferriero DM, Fullerton HJ, Bernard TJ, et al. Management of Stroke in Neonates and Children: A Scientific Statement From the American Heart Association/American Stroke Association. Stroke. 2019;50(3):e51-e96. doi:10.1161/STR.0000000000000183
  30. Cauldwell M, Rudd A, Nelson-Piercy C. Management of stroke and pregnancy. Eur Stroke J. 2018;3(3):227-236. doi:10.1177/2396987318769547
  31. Talahma M, Strbian D, Sundararajan S. Sickle Cell Disease and Stroke. Stroke. 2014;45(6):e98-e100. doi:10.1161/STROKEAHA.114.005144
  32. Hong I, Karmarkar A, Chan W, et al. Discharge Patterns for Ischemic and Hemorrhagic Stroke Patients Going from Acute Care Hospitals to Inpatient and Skilled Nursing Rehabilitation. Am J Phys Med Rehabil. 2018;97(9):636-645. doi:10.1097/PHM.0000000000000932

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.

Hypokalemic Periodic Paralysis in the ED

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

Case Presentation

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

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

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

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

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

ECG-hypokalemia

Hypokalaemia

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

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

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

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

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

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

The differential diagnosis for weakness in lower limb include :

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

References

[cite]

Triads in Medicine – Rapid Review for Medical Students

triads in medicine
~ Sumaiya Hafiz, UAE ~ Leave a comment

One of the most convenient ways of learning and remembering the main components of disease and identifying a medical condition on an exam are Triads, and medical students/interns/residents swear by them.

Be it a question during rounds, a multiple-choice exam question to be solved, or even in medical practice, the famous triads help physicians recall important characteristics and clinical features of a disease or treatment in an instant.

Since exam season is here, this could serve as a rapid review to recall the most common medical conditions.

While there are a vast number of triads/pentads available online, I have listed the most important (high-yy) ones that every student would be asked about at least once in the duration of their course.

1) Lethal Triad also known as The Trauma Triad of Death
Hypothermia + Coagulopathy + Metabolic Acidosis

2) Beck’s Triad of Cardiac Tamponade
Muffled heart sounds + Distended neck veins + Hypotension

3) Virchow’s Triad – Venous Thrombosis
Hypercoagulability + stasis + endothelial damage

4) Charcot’s Triad – Ascending Cholangitis
Fever with rigors + Right upper quadrant pain + Jaundice

5) Cushing’s Triad – Raised Intracranial Pressure
Bradycardia + Irregular respiration + Hypertension

6) Triad of Ruptured Abdominal Aortic Aneurysm
Severe Abdominal/Back Pain + Hypotension + Pulsatile Abdominal mass

7) Reactive Arthritis
Can’t See (Conjunctivitis) + Can’t Pee (Urethritis) + Can’t Climb a Tree (Arthritis)

8) Triad of Opioid Overdose
Pinpoint pupils + Respiratory Depression + CNS Depression

9) Hakims Triad – Normal Pressure Hydrocephalus
Gait Disturbance + Dementia + Urinary Incontinence

10) Horner’s Syndrome Triad
Ptosis + Miosis + Anydrosis

11) Mackler’s Triad – Oesophageal Perforation (Boerhaave Syndrome)
Vomiting + Lower Thoracic Pain + Subcutaneous Emphysema

12) Pheochromocytoma
Palpitations + Headache + Perspiration (Diaphoresis)

13) Leriche Syndrome
Buttock claudication + Impotence + Symmetrical Atrophy of bilateral lower extremities

14) Rigler’s Triad – Gallstone ileus
Gallstones + Pneumobilia + Small bowel obstruction

15) Whipple’s Triad – Insulinoma
Hypoglycemic attack + Low glucose + Resolving of the attack on glucose administration

16) Meniere’s Disease
Tinnitus + Vertigo + Hearing loss

17) Wernicke’s Encephalopathy- Thiamine Deficiency
Confusion + Ophthalmoplegia + Ataxia

18) Unhappy Triad – Knee Injury
Injury to Anterior Cruciate Ligament + Medial collateral ligament + Medial or Lateral Meniscus

19) Henoch Schonlein Purpura
Purpura + Abdominal pain + Joint pain

20) Meigs Syndrome
Benign ovarian tumor + pleural effusion + ascites

21) Felty’s Syndrome
Rheumatoid Arthritis + Splenomegaly + Neutropenia

22) Cauda Equina Syndrome
Low back pain + Bowel/Bladder Dysfunction + Saddle Anesthesia

23) Meningitis
Fever + Headache + Neck Stiffness

24) Wolf Parkinson White Syndrome
Delta Waves + Short PR Interval + Wide QRS Complex

25) Neurogenic Shock
Bradycardia + Hypotension + Hypothermia

Further Reading

[cite]

Acute Ischemic Stroke Management in the ED – Part 1

Acute Ischemic Stroke Management
~ Jule Santos, Brasil ~ Leave a comment

Your shift has just started, and you received a 56-year-old female patient, brought by her family due to a sudden loss of movement. The patient seems awake; you approach her, introduce yourself, and ask for her name. She does not understand. You ask her to look at you and to raise her arms, then you see: the left side of her body was paralyzed. In your head, a stroke sign lights up: you need to decide whether to activate the stroke protocol immediately or not, after all:

Time Is Brain

Important Hints

  • Know the protocols and references of your hospital and your region for acute stroke management. Your Emergency Department should be prepared to suspect of stroke in any patient presenting with acute neurological deficits and have a pre-established protocol for prioritizing care.

  • The prehospital service (EMS) should provide notification to the receiving hospital that a suspected stroke patient in the therapeutic window is en route and direct the patient to the closest hospital with thrombolytic support.

  • By AHA/ASA recommendations, door-to-needle time <60 minutes should be sought in more than 50% of patients treated with alteplase (tPA) (1)

Neurons are very sensitive to changes in brain flow and die within minutes in the absence of perfusion: thus the urgency in attempting rapid reperfusion. (2)

Do not delay the patient evaluation because the emergency department is overcrowded! Move the patient to a monitored bed as soon as possible.

While the patient is being monitored, continue your focused neurological examination quickly and accurately. Asking for the patient to lift and hold the arms, then the legs, tests sensitivity and strength. Then you should ask her to try to smile, assess the eye movement, pupils, search for nystagmus, and ask her to try to expose the tongue, assessing movement and understanding. You ask her simple questions: full name, date, where she is, point to a cell phone, a mug and a watch and ask if she recognizes them. At the same time, you evaluate strength, orientation and deficits.

VITAL SIGNS
Blood Pressure: 180/110 mmHg
Pulse: 125 bpm
SatO2%: 98
Respiratory Rate: 18 bpm

Do not forget to measure capillary GLUCOSE (135mg/dl). Important to rule out other causes of neurological symptoms that can mimic a stroke.

Hypoglycemia

Hypoglycemia is the first condition we evaluate for when the patient presents with acute neurological deficit, decreased level of consciousness, weakness, syncope, convulsion, etc. Hypoglycemia is defined by a blood glucose level less than 45 mg/dl. Symptoms improve rapidly as soon as corrected in most cases. However, it may take time for a complete improvement, and does not always rule out a stroke. (3)

Seizure

Seizure and post-ictal condition are also conditions that can mimic a stroke. Todd’s Paralysis is a focal weakness localized to one side of the body, which occurs around 13% of seizures. These deficits usually last up to 20 minutes but may last 48 hours. Unfortunately, seizures may present in the setting of acute stroke or patients with a stroke history due to neuronal damage. (3)

Stroke Mimics

Stroke mimics are common, accounting for 5% to 31% of patients with acute focal neurological deficit. (3) Diagnosis is not always simple, and abnormal eye movements, increased diastolic blood pressure greater than 90mmHg, and history of atrial fibrillation or angina are most commonly found in stroke. In the presence of decreased level of consciousness, cognitive dysfunction and normal eye movements are more common in stroke mimics.

Stroke Mimics

Condition

Misdiagnosed as stroke (%)
Brain tumor
7-15
Labyrinthitis
5-6
Metabolic disorder
3-13
Migraine
11-47
Psychiatric disorder
1-40
Seizures
11-40
Sepsis
14-17
Syncope
5-22
Transient global amnesia
3-10
Other
11-37

From Konrad CN, Crocco T, Biola J, Larrabee H. Is it stroke, or something else? The Journal of Family Practice. 2010 Jan; 59 (1): 26-31.

The time is ticking, and you must make critical decisions.

  • Is it a stroke? Or a disease with an acute neurological symptom that mimics a stroke?

  • I need a brain imaging study in less than 20 minutes. (2) Will I need to protect the patient's airway before, or should I go straight to the imaging exam?

  • What brain imaging study do I have and what should I do first? CT or MRI?

  • Is there an indication for IV alteplase? Should I do it in my unit, or should I referral the patient to another center?

  • Are there indications for mechanical thrombectomy? Should I do CT angiography at the same time?

Management of acute stroke will depend on:

  • The support you have.
  • Time of onset of the stroke, that is, duration of symptoms.
  • The severity of symptoms:
    • Physical examination: NIHSS, etc.
    • Signs of a large vessel stroke
    • Area of irreversible ischemia “core” versus penumbra area, salvageable area
  • The desire of the patient/family after being informed of the risks/benefits.

Clinical History

The clinical history must be acquired quickly and directly. Essential points: time of symptoms, associated symptoms, comorbidities, and medications of continuous use.

It is important to note that the time of the symptom is counted from the last time the patient was seen without symptoms and not when someone noticed the deficit. (1) If the patient woke up with the deficit, time counts from when he/she was seen without symptoms (e.g., the day before bedtime).

Laboratory, Imaging, Management

Unnecessary tests should not delay brain imaging. It should be performed within 20 minutes of the patient’s arrival at the hospital!

If you do not have a CT scanner in your hospital, the patient should be referred for a center that has one, preferably with a stroke unit. In this situation, physical examination and accurate data of the clinical history must be passed to the place of reference. A physician should accompany the patient.

Treatment of blood pressure only if BP> 220 x 110mmHg, preferably with easy-to-control intravenous medication (labetalol, nicardipine, sodium nitroprusside, etc.). Avoid oral medications due to bronchospasm risk and unpredictable effect. Not having intravenous options, I would consider tolerating hypertension until the diagnosis is confirmed.

Venous access with the collection of samples such as complete blood count, electrolytes, renal function, TAP, APTT, troponin, and more as needed, according to patient comorbidities and medications.

Do not delay the brain image waiting for the collection of laboratory tests. Do not delay imaging or therapy with tPA expecting laboratory test results, unless it is essential.

Venous access before the examination is essential if there is a decision to perform CT angiography of cervical and intracranial vessels in the possibility of mechanical thrombectomy. However, performing CTA should not delay the performance of chemical thrombolysis if indicated. That is, the radiology sector should be prepared to perform immediately after CT if indicated.

Which imaging test is the best? and Why?

MRI

Weighted MRI diffusion shows a greater positivity than CT in the first 24 hours for ischemic stroke, especially in the vertebrobasilar territory. However, its role in ED is still limited because of its uncertain accuracy for the diagnosis of acute hemorrhage, low immediate availability, patient contraindications (not cooperating, claustrophobia, metal implants, pacemaker, etc.) and cost-effectiveness.

CT

CT without contrast, is relatively accessible in most reference centers. It discards other causes of neurological deficit such as ICH, abscess, brain tumor, etc. It may not diagnose acute stroke. But together with a compatible clinical story, it is the only necessary brain image for performing IV alteplase. (2)

Every patient with acute neurological deficit, independent of time, must perform a brain imaging, mainly to rule out other causes, such as ICH, which completely changes the treatment.

All patients with acute neurological deficits, mainly without a diagnosis, must be accompanied by a physician assistant during transfer to imaging, due to the risk of abrupt change/worsening of the clinical status.

It is important to have communication between the ED areas, to warn the radiology department in advance that the patient is on the way, and that the exam should be prioritized. (2)

You accompany the patient during the CT scan. And this is her exam:

Do the best you can, ask for help when in doubt, study and care with love.

To Be Continued.

References and Further Reading

  1. Tintinalli, Judith E.,, et al. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. Eighth edition. New York: McGraw-Hill Education, 2016.
  2. William J. Powers et al. 2018 Guidelines for the Early Management of Patients With Acute Ischemic Stroke. AHA/ASA Guideline. 2018 Mar;49(3):e46-e110. doi: 10.1161/STR.0000000000000158. Epub 2018 Jan 24.
  3. Brit Long, MD, Stroke Mimics: Pearls and Pitfalls, http://www.emdocs.net/stroke-mimics-pearls-and-pitfalls/ em 07/05/2019
[cite]

AMS and right side weakness

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In case you didn’t encounter acute altered mental status and right side weakness today!

690.1 - Figure 6a. CT - Left basal ganglia infarct
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Acute Ischemic Stroke chapter is just added

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692.4 - Left parietooccipital cortex subcortical white matter infarct

Acute Ischemic Stroke chapter written by Fatih Büyükcam from Turkey is just uploaded to the Website!

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