Intracerebral Hemorrhage (2024)

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

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.

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.

Basics of Bleeding Control (2024)

by Tasnim Ahmed & Abdulla Alhmoudi

Introduction

The primary objective in the resuscitation of traumatic hemorrhage is to achieve effective hemostasis and maintain hemodynamic stability. The severity of bleeding depends on the depth of the wound and the type of injured vessel. The approach to bleeding control should be tailored to the type and size of the bleeding vessel and the specific anatomical regions involved. Delayed or ineffective haemorrhage management can complicate the healing process and, in severe cases, lead to fatality. Extremity haemorrhage has historically contributed significantly to high mortality rates from casualties during wars [1]. Therefore, the prompt implementation of appropriate haemostatic techniques is a crucial aspect of efficient trauma management. This critical task is typically initiated by the prehospital team and followed by more advanced, invasive techniques provided by the trauma team in a controlled hospital setting

Types of Wounds

Wound is an impairment to the structural integrity of biological tissues, including the skin, mucous membranes, and organ tissues. This disruption in tissue integrity may arise from a diverse range of causes, including traumatic injuries, pathological processes, or surgical interventions. Metric parameters such as size (length), depth, shape, and whether they are open or closed are used to describe wounds.

The subsequent descriptors represent the terminology utilized for the classification of wounds:

Contusions

Contusions result from perpendicular blunt force to the skin, usually through a layer of clothes. Rupture of subcutaneous capillaries can occur, resulting in the formation of a hematoma (Figure 1). The recommended management for this type of wound consists of analgesics and following the “RICE” protocol (Rest, Ice, Compression, and Elevation) [2].

Figure 1 - Contusion

Abrasion

Abrasion is the scraping or scratching of the surface layers of skin (epidermis) when subjected to oblique forces (Figure 2). Proper wound care involves cleansing the wound, applying a sterile bandage, administering analgesics, ensuring tetanus protection, and implementing the RICE protocol [2].

Figure 2 - Abrasion

Incision

Incision is defined as a cut that features straight edges along the margins of the wound. It can be caused by sharp objects like scalpels, knives, sharp metal pieces, or glass (Figure 3). Tissue loss is uncommon, and the wound margins can be easily aligned for closure with medical glue or sutures [1,2,3].

Figure 3 - Incision

Lacerations

Characterized irregular or jagged edges, appearing torn rather than neat incisions [1,3]. They can have an irregular or linear direction and may branch out (Figure 4). Objects with broken or serrated edges or blunt impact on tissue overlying bone typically cause lacerations. Treatment approaches for lacerations are similar to those for incision wounds. However, the appropriate subspecialty should manage deep, complex lacerations or those involving sensitive areas like the face, joints, or tendons.

Figure 4 - Laceration

Avulsion

Avulsion involves a full-thickness laceration-type wound, which usually creates a flap of tissue (Figure 5) [1,3]. Mechanical accidents involving fingers (degloving injuries) can cause avulsions. More severe cases may include exposure of internal organs. Avulsions are challenging to repair and should never be considered minor injuries.

Figure 5 - Avulsion

Amputation

Amputations differ from avulsions in that they involve the complete loss of a limb, whereas avulsions result in the loss of just a flap of skin (Figure 6). It can occur at any point along an extremity and is usually accompanied by significant arterial bleeding. Despite the seriousness of this injury, a properly cooled and transported amputated limb may sometimes be surgically reattached in a hospital setting.

Figure 6 - Amputation

Puncture and Penetrating Wounds

Puncture and penetrating wounds result from the penetration of a sharp object into the tissue without lateral movement from the point of entry (Figure 7). Puncture wounds can be deceptive, as they may appear small on the surface but extend deeply, potentially damaging the neurovascular structure or internal organs and causing significant internal bleeding or secondary injuries. 

Figure 7 - Puncture wound with soft tissue infection

Stab wounds from knives or sharp objects, as well as bullet wounds, are examples of penetrating injuries [1,2,3]. Occasionally, the penetrating object may remain logged to the injury and should never be removed without careful assessment by the trauma team, as it might act as mechanical hemostatic and result in further bleeding once removed. 

Site of Injury

Injuries can also be classified into three types, depending on the injured site of the body; each entails a different approach to management. Extremity injuries refer to damage inflicted on the blood vessels of the arms or legs. Junctional injuries, on the other hand, involve vascular damage occurring at the junction where the extremities meet the torso, such as the hip, axilla, or base of the neck. Torso injuries often involve non-compressible truncal hemorrhage that occurs anywhere on the torso and involves large blood vessels.

Vascular Injury

Injury to any blood vessel type can result in external bleeding. The specific type of vascular injury can be identified based on the characteristics of bleeding observed [1,2,4].

The following are the distinct types of vascular injuries and their corresponding patterns of bleeding:

Arterial Bleeding

Arterial bleeding typically occurs as a consequence of deep penetrating injuries or amputations. It is distinguished by the forceful ejection of bright red blood from the wound synchronized with each heartbeat [2]. Complete laceration of the artery may trigger spontaneous constriction, which helps to control bleeding. However, if only the artery wall is damaged without complete dissection, it can lead to persistent bleeding.

Indicators of arterial injury are classified into hard signs and soft signs [2]. Identifying hard signs indicates an immediate need for arterial exploration and surgical intervention. To aid in the recollection of these hard signs, the mnemonic “The Broken PIPE” can be employed (Box 1). Conversely, soft signs indicate the necessity for additional investigations such as ankle-brachial index measurement, Duplex Doppler ultrasound, or CT angiography, as determined by clinical assessment. The soft signs can be represented by the mnemonic “NON-Deadly HemorrHage” (Box 2).

Venous Bleeding

Venous Bleeding is characterized by a slower flow of dark red blood out of the wound [2]. However, caution is still recommended in venous bleeding, as it can contribute to significant and rapid bleeding if left untreated [4].

Capillary Bleeding

Capillary Bleeding usually results from damage to subcutaneous capillaries. It is characterized by slow, intermittent bleeding in the form of dots or small oozing [2,4].

Indications of Bleeding Control Techniques

Achieving hemodynamic stability necessitates the effective control of all life- or limb-threatening bleeding. While in most cases of traumatic and non-traumatic resuscitation, emphasis is placed on managing the airway and ensuring proper breathing, in situations of exsanguinating bleeding, prioritizing massive hemorrhage control surpasses the immediate focus on airway and breathing management [1]. The choice of hemostatic technique should be based on the depth and specific location of the injury, as outlined in detail in the “Bleeding Control Techniques” section below.

Contraindications of Bleeding Control Techniques

There are no absolute contraindications to any specific hemostatic method [1]. However, bleeding injuries should not distract the physician from managing concurrent immediate life-threatening conditions. Additionally, immediate wound closure is not recommended in wounds older than 8 hours. Instead, these types of wounds should be cleaned thoroughly, covered with sterile dressing, and closed after 3-5 days if there are no signs of infection. This is referred to as “delayed primary closure” [2,3].

Preparation

Similar to all medical procedures, thorough preparation is essential to ensure efficient hemostasis. This preparation encompasses the healthcare team, equipment, medications, the patient, and the wound.

Team Preparation

The healthcare providers involved in the procedure should possess comprehensive knowledge of indications, contraindications, techniques, and potential complications. The team should wear appropriate personal protective equipment, including face masks, face shields, surgical gowns, gloves, and shoe covers as necessary [3]. This protective gear is crucial to safeguard against blood splashes and potential contact with body fluids, particularly in trauma settings where the patient’s health status may be unknown.

Equipment Preparation

The equipment and medications used for hemostasis must be meticulously prepared and checked for the expiry date and functionality. The required equipment is listed under the corresponding techniques in the “Bleeding Control Techniques” section below.

Patient Preparation

A detailed explanation of the procedure should be provided to the patient, and informed consent should be obtained if applicable. Additionally, securing intravenous access and collecting a blood sample for type and cross-matching and coagulation profile are imperative. Administering analgesics and local anesthetics before procedural maneuvers helps to effectively minimize patient discomfort and disruptive movements.

Wound Preparation

A thorough assessment of the wound should be conducted. Distal movement and neurovascular function should be assessed prior to any manipulation. Contaminated wounds require proper irrigation to remove foreign bodies, followed by sterilization of the surrounding skin using antiseptic solution such as povidone iodine or chlorhexidine. However, wound preparation should not delay definitive hemostatic measures [1,3]. 

Bleeding Control Techniques

Direct Pressure

The initial step in controlling bleeding involves applying direct pressure to the bleeding wound. This facilitates the formation of a platelet plug and the initiation of the physiologic coagulation cascade, which is typically achievable within 10 to 15 minutes of proper pressure application [1]. 

Equipment

  • Sterile gauze pad size 4×4
  • Compression bandage
  • Splint\brace

Technique

Ensuring the proper replacement of skin flaps is essential, followed by placing multiple 4×4 sterile gauzes, ideally low adherent type, with equal pressure applied. The wound can be wrapped with a compression bandage if it is in the head or extremities. Following the application of a compression bandage to the extremities, distal mobility, sensation, and perfusion should be checked. Limbs should be placed in a brace to minimize movement and keep it elevated. In body junctions, the wound can alternatively be packed with gauze or hemostatic agents along with topical pressure application [1,2,4].

Precautions

It is important to avoid removing soaked gauze, as this can function as a foreign clot; instead, a new gauze should be applied on top of the existing ones [4]. Compression bandages should be avoided in thoracic wounds, as they can constrict breathing.

Pressure on Arteries

When the source of bleeding cannot be identified, applying proximal pressure can help control the bleeding by reducing blood flow to the injured artery [1].  This is only feasible with extremity wounds and should not be applied to the carotid artery, as this can precipitate ischemic brain insult or vagal stimulation, resulting in bradycardia [4].

Precautions

The time of application is limited to 10 minutes due to the risk of tissue necrosis distal to the pressure point.

Tourniquet

The indication to use tourniquets is severe extremity bleeding that is not controlled by direct pressure application. The concept is constricting arterial flow to the injured area. It is an extremely painful procedure, and proper analgesia should be ensured before applying a tourniquet if time allows.

Equipment

  • Proper size tourniquet
  • Alternative: Blood pressure cuff

Technique

Remove any clothing obstructing the tourniquet application site, ensuring it is directly applied to the skin and remains visible. Position the tourniquet approximately 2-3 inches above the wound, avoiding joints (Figure 8). Tighten the tourniquet until the bleeding stops and the pulse distal to the tourniquet is no longer palpable. Note the time of placement on the tourniquet tag or consider using an indelible marker to write it on patient’s skin. [4,5].

Figure 8 - Tourniquet application

If bleeding is not controlled and the distal pulse is still present after applying the first tourniquet, apply a second one just above its location [4]. Increasing the width of the second tourniquet is more effective in controlling bleeding and reducing complications than excessively tightening the initial one. Administer analgesia as needed after the tourniquet is applied.

An alternative to the tourniquet is applying a blood pressure cuff proximal to the wound. The cuff is then inflated 20-30 mm Hg above systolic blood pressure or over 250 mm Hg, and the tubing is clamped with a hemostat [2]. There are many ways to improvise a tourniquet using non-stretchable clothing and a windlass rod like a pen; however, a commercially designed tourniquet is preferable and not likely to loosen easily with patient movement. 

To safely remove the tourniquet, apply a pressure dressing directly onto the wound. Then, gradually release the tourniquet while carefully monitoring for any signs of bleeding. If bleeding is successfully controlled, keep the tourniquet loosely secured in case of potential re-bleeding. If bleeding recurs, reapply firm pressure by tightening the tourniquet [5].

Precautions

The maximum duration for tourniquet application is 120 minutes [2]. Prolonged tourniquet application can lead to complications such as nerve injury, tissue necrosis, compartment syndrome, and rhabdomyolysis. However, if the extremity is amputated or if the tourniquet has been applied for more than 6 hours, it should not be loosened as permanent muscle damage occurs after 6 hours and might require amputation.1 Moreover, potential reperfusion injury may occur after 60 minutes of tourniquet use, leading to inflammation-induced damage in local areas and systemic effects on vital organs caused by inflammatory mediators [5].

Topical Hemostatic Agents

Another alternative or adjunct to tourniquet use is topical hemostatic agents. These agents create a platform for platelet deposition and facilitate hemostasis [6]. Examples include [1] oxidized cellulose (e.g., Surgicel), dry gelatin (e.g., Gelfoam, Surgifoam), or cyanoacrylate.

Equipment

  • Hemostatic agent (e.g., Combat Gauze, Celox Gauze, or ChitoGauze)
  • Pressure dressing

Technique

The hemostatic gauze is applied with direct pressure for at least 3 minutes. After the field dries, the wound can be sutured, or pressure dressing can be applied. It is important to note that a dry field is required to apply the cyanoacrylate type. Pressure or tourniquet should be used before its application. An alternative to hemostatic gauze is topical thrombin. It can be used directly or diluted with saline and sprayed onto the wound. A concentration of 100 units/mL is effective. In severe bleeding, a concentration of 1000 to 2000 units/mL can be used [1].

Precautions

Potential complications associated with hemostatic agents include excessive granulation tissue and fibrosis with absorbable gelatin agents or foreign body reaction with cellulose [1,7].

Balloon Catheter

Balloon catheters can be used as an improvised tamponade technique to temporarily control severe bleeding from deep injuries, when other conventional methods fail [1,8].

Equipment

  • Fogarty catheters, Foley catheters, or Sengstaken-Blakemore tubes.
  • 10 cc syringe

Technique

The tube is blindly inserted into the wound, then the ballon is inflated to halt bleeding from deep vascular injuries [1].

Suture Ligation

Suture ligation is used for controlling large bleeding vessels. An effective ligation technique requires careful examination and knowledge of the vascular anatomy to trace and identify the sources of bleeding. A retracted artery can be a potential source of delayed bleeding. Therefore, once an injured vessel is identified, the opposite end should also be traced and ligated [1]. 

Equipment

  • Blood pressure cuff
  • Absorbable suture (e.g., Vicryl, Monocryl, and PDS).
  • Haemostat
  • Needle holder
  • Scissors

Technique

A blood pressure cuff is placed proximally and inflated until the bleeding stops to create a clear field. With gradual deflation of the cuff, large bleeding vessels will start to be visible. Ligation is then completed with suturing in the following steps: [1]

  1. Using a haemostat pinch the free end of the bleeding vessel.
  2. Wrap a proper-sized suture around the vessel.
  3. Tie the suture at the base of the vessel.
  4. Release the haemostat carefully (Figure 9).

if the vessel can not be seen, a figure 8 suture can be applied (Figure 10) [1,3]. 

Figure 9 - Vessel ligation technique. (1) Grasp the cut end of the bleeding vessel with a haemostat. (2) Pass an appropriately sized suture around the vessel. (3) Tie and secure the suture around the base of the bleeding vessel. (4) Gently release the haemostat from the blood vessel. (Freeman C, Reichman EF. Hemorrhage Control. In: Emergency Medicine Procedures. 6th ed. Elsevier; 2020:112-1. "Control of the Bleeding Vessel that is Visualized." Adapted and redrawn by Tasnim Ahmed, MD).
Figure 10. Figure 8 stich. A. Needle directions, B.Tie. (Freeman C, Reichman EF. Hemorrhage Control. In: Emergency Medicine Procedures. 6th ed. Elsevier; 2020:112-2. "Control of a Bleeding Vessel Deep or Embedded in Tissue." Adapted and redrawn by Tasnim Ahmed, MD).

Cauterization

Cauterization is cost effective and simple haemostatic technique for small vessels measuring less than 2 mm in diameter. Electrical cauterization  involves using electrical current to heat an electrode, which then is used to thermally burn the vessel wall and seal it with charred tissue [1,10]. 

Chemical cauterization can be achieved using silver nitrate (AgNO3). This involves applying the agent to the vessel wall using an applicator, typically a long and small wooden stick tipped with the silver nitrate. Silver nitrate reacts with proteins in the tissue, forming an insoluble deposit that blocks the blood flow. It is only effective when applied to a dry tissue or minimal oozing [1]. 

Equipment

  • Blood pressure cuff
  • Silver nitrate or electric cautery

Technique

Position a blood pressure cuff proximally and gradually inflate it until bleeding stops, to achieve a clear field. Then gently release the pressure, until the smaller bleeding vessels become visible. Use the electrocautery to burn the end of the bleeding vessel or rub the silver nitrate against it to achieve an artificial clot [1].

Vasoconstrictors

In normal conditions, small vessels spontaneously stop bleeding. However, if bleeding persists, local vasoconstrictors mixed with local anaesthetics can be applied. Local anesthetic solutions containing epinephrine, such as lidocaine and bupivacaine, are readily available in the Emergency Department.

Equipment

  • 10 cc syringe
  • Epinephrine 1:1000
  • Saline-soaked gauze

Technique

Prepare the diluted epinephrine in a 10 cc syringe. Aspirate prior to injection to ensure that the solution is not injected into a blood vessel. Inject 1 to 2 mL of the solution around the bleeding vessel. Apply direct pressure with saline soaked gauze over the wound. Alternatively, spray the wound with the diluted solution. [1,3]

Precautions

It’s important to avoid using epinephrine or other vasoconstrictors in end-arterial areas like fingers, toes, ears, nose, or penis, to avoid organ ischemia.

Complications

Complications arise when the above-listed techniques are either overused or applied inappropriately. For detailed information regarding the particular complications associated with each technique, please refer to the corresponding technique’s “Precautions” section.  

Special Patient Groups

Obtaining hemostasis might be challenging in patients with coagulopathy. Therefore, it is important to remain vigilant and promptly assess the platelet count and plasma coagulation profile (PT/PTT/INR) in patients experiencing external bleeding. The early administration of tranexamic acid, blood products, and cryoprecipitate can aid in achieving hemostasis.

Authors

Picture of Tasnim Ahmed

Tasnim Ahmed

Emergency Medicine Residency graduate from Zayed Military Hospital, Abu Dhabi, UAE. Deputy Editor-in-Chief of the Emirates Society of Emergency Medicine (ESEM) newsletter. Senior Board Member and Website Manager of the Emirates Collaboration of Residents in Emergency Medicine (ECREM). Awarded Resident of the Year twice, at ESEM23 and Menatox23. Passionate about medical education, with a focus on blending art and technology into innovative teaching strategies.

Picture of Abdulla Alhmoudi

Abdulla Alhmoudi

Dr Abdulla Alhmoudi is a Consultant Emergency Medicine, serving at Zayed Military Hospital and Sheikh Shakhbout Medical City - Abu Dhabi. He pursued his residency training in Emergency Medicine at George Washington University in Washington DC and further enhanced his expertise with a Fellowship in Extreme Environmental Medicine. Dr Alhmoudi's passion for medical education is evident in his professional pursuits. He currently holds the position of Associate Program Director at ZMH EM program and is a lecturer at Khalifa University College of Medicine and Health Sciences. Beyond medical education, he maintains a keen interest in military medicine and wilderness medicine.

Listen to the chapter

References

  1. Chapter 112. Hemorrhage Control. In: Reichman EF. eds. Emergency Medicine Procedures, 2e. McGraw Hill; 2013. Accessed May 22, 2023. https://accessemergencymedicine.mhmedical.com/content.aspx?bookid=683&sectionid=45343754
  2. Spehonja A, Prosen G. Basics of Bleeding Control. In: Cevik AA, ed. International Emergency Medicine Education Project. iEM Education Project; 2018:598-601.
  3. Lammers RL, Smith ZE. Principles of wound management. In: Roberts JR, Hedges JR, eds. Roberts & Hedges’ Clinical Procedures in Emergency Medicine. 6th ed. Philadelphia, PA: Elsevier; 2014:611-634.
  4. Department of the Navy. Bleeding. Brooksidepress.org. 2001. Accessed May 22, 2023. https://www.brooksidepress.org/Products/OperationalMedicine/DATA/operationalmed/Manuals/Standard1stAid/chapter3.html.
  5. Lee C, Porter KM, Hodgetts TJ. Tourniquet use in the civilian prehospital setting. Emergency Medicine Journal. 2007;24(8):584-587. doi:10.1136/emj.2007.046359
  6. Sileshi B, Achneck HE, Lawson JH. Management of surgical hemostasis: topical agents [published correction appears in Vascular. 2009 May-Jun;17(3):181]. Vascular. 2008;16 Suppl 1:S22-S28.
  7. Levy JH. Hemostatic agents and their safety. J Cardiothorac Vasc Anesth. 1999;13(4 Suppl 1):6-37.
  8. Feliciano DV, Burch JM, Mattox KL, Bitondo CG, Fields G. Balloon catheter tamponade in cardiovascular wounds. Am J Surg. 1990;160(6):583-587. doi:10.1016/s0002-9610(05)80750-0
  9. Rudge WB, Rudge BC, Rudge CJ. A useful technique for the control of bleeding following peripheral vascular injury. Ann R Coll Surg Engl. 2010;92(1):77-78. doi:10.1308/rcsann.2010.92.1.77
  10. Kamat AA, Kramer P, Soisson AP. Superiority of electrocautery over the suture method for achieving cervical cone bed hemostasis. Obstet Gynecol. 2003;102(4):726-730. doi:10.1016/s0029-7844(03)00622-7

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.

Question Of The Day #44

question of the day

Which of the following is the most appropriate next investigation to confirm this patient’s diagnosis?

This patient presents to the Emergency Department with altered mental status.  This presenting symptom can be due to a large variety of etiologies, including hypoglycemia, sepsis, toxic ingestions, electrolyte abnormalities, stroke, and more.  The management and evaluation of a patient with altered mental status depends on the primary assessment of the patient (“ABCs”, or Airway, Breathing, Circulation) to identify any acute life-threatening conditions that need to be managed emergently, the history, and the physical examination.  One mnemonic that may help in remembering the many causes of altered mental status is “AEIOUTIPS”.  The table below outlines this mnemonic.

ALTERED MENTAL STATUS

The information provided indicates that the patient’s headache was maximal at onset, severe, associated with vomiting, and led to a deteriorating mental status ultimately requiring intubation.  This history is very concerning for intracranial bleeding, especially subarachnoid hemorrhage (SAH).  The majority of atraumatic SAHs are caused by the rupture of a saccular aneurysm.  This causes the leakage of blood into the subarachnoid space.  Symptoms of a SAH are sudden onset headache that is maximal intensity at onset (“thunderclap headache”), syncope, vomiting, seizures, and any neurological deficits.  Risk factors for SAH are age over 50years-old, family history of SAH, alcohol abuse, tobacco smoking, Marfan Syndrome, Ehlers-Danlos Syndrome, and Polycystic Kidney Disease.  Diagnosis of SAH takes into account the patient’s history, physical exam, and risk factors. 

Patients that arrive in the Emergency Department under 6hours since symptom onset should initially get a noncontrast CT scan of the head (Choice D).  When a noncontrast head CT is performed in this time window, its sensitivity reaches 98-100%.  Noncontrast head CTs performed within the first 24hrs since headache onset have a sensitivity of about 90%.  Patients with signs and symptoms concerning for SAH who have a negative CT head should get a lumbar puncture (Choice A) to evaluate for xanthochromia.  This is especially important if the patient’s symptoms have been for over 6 hours.  A 12-lead EKG (Choice B) can show ST and T wave changes, but an EKG alone cannot be used to make a diagnosis of SAH.  A brain MRI (Choice C) can make the diagnosis of SAH, but a CT scan would be preferred due to greater CT scan accessibility, cost, and the shorter time of this imaging test.  The best next investigation would be a noncontrast CT of the head (Choice D).

Correct Answer: D

References

[cite]

Epidural Hematoma

epidural hematoma

Authors: Kilalo Maeli Mjema, Emergency Physician and Mugisha Clement, Neurosurgeon.

Case Presentation

A 34 years old male sustained a traumatic brain injury following a motor vehicle accident 3 hours before presentation to ED. BP: 117/69mmHg. HR: 84, RR: 18, SPO2: 99% in room air, T: 36.9.

Primary Survey

Airway: patent and protected
Breathing: bilateral equal air entry
Circulation: warm extremities, 1 second capillary refill time
Disability: alert and oriented, pupils 4mm bilaterally equally reactive to light, RBG 5.6 mmol/L
Exposure: raccoon right eye, bruises on the forehead and upper limbs

SAMPLE History

Signs and symptoms: mostly chest pain than the headache, nausea
Allergies: no known allergies
Medication: had received tramadol, dexamethasone, tetanus toxoid and some intravenous fluids before being referred to our facility
Past medical history: no known comorbid or any significant history
Event: sustained motor vehicle accident as a motorcycle driver with no helmet on 3 hours prior presentation, associated with a 20 minutes loss of consciousness. Attended at another facility where he regained his full consciousness, wounds dressed, medication given as above, E-FAST negative and CT imaging done. He remained conscious throughout and was transferred for neurosurgical observation and interventions.

Neuro-observation and continuous monitoring were planned. Blood samples sent for CBC, PT, aPTT, blood type and crossmatch. The neurosurgical review was done, and the patient was to be kept inpatient for close neurosurgical observation and interventions as needed.

Patient progress while still in the ED

In the course of stay in the ED, the patient started to vomit, became drowsier overtime, was moving mostly the right side of his limbs. The right pupil was 6-7mm non-reactive to light and GCS dropped to E1M4(Rt)V2

Vitals

BP 133/79 mmHg HR 39-45 bpm RR 14 rpm SPO2 99% in room air.

The patient was emergently transferred for repeat imaging and prepared for emergency craniotomy and hematoma evacuation. Theatre was informed and ready to receive the patient.

Rapid sequence induction and intubation 

  • Patient pre-oxygenated
  • Induction with iv ketamine 2mg/kg (weight 75kg)
  • Paralyzed with iv suxamethonium 100mg 
  • Intubated by sized 8 cuffed ETT

Mannitol 20g iv infusion was given over 10 minutes.

Intraoperative Findings and Progress

Right frontotemporoparietal craniotomy was done. Approximately 100 mls of hematoma because of spurting bleeding from the medial meningeal artery was found.  No other obvious identifiable bleeding was seen. Hemostasis was achieved and closed in layers with a drain. The patient had a complete neuro improvement, extubated at day 5 and discharged 9th day.

Clinical Pearls

  • The incidence of epidural hematoma is highest among adolescents and young adults
  • Most cases are a result of head trauma by traffic accidents, falls or assaults
  • Most commonly due to middle meningeal arterial bleed
  • Epidural hematoma does not cross suture margins but crosses dural attachments as a convex lens shaped appearance
  • Lucid intervals are seen in patients
  • Watch for raised intracranial pressure; ipsilateral dilated pupil, Cushing reflex, altered mentation, vomiting
  • Glucocorticoids have no role in reducing cerebral edema in traumatic brain injury
  • In the presence of epidural hematoma with the feature of herniation, mannitol can be given with caution that craniotomy and evacuation is going to be done immediately
  • Ketamine in RSII can still be considered in traumatic brain injury where blood pressures are not raised

Clinical Pearls

In the context of non-operative management, properly monitoring neurologic status and progress is the key factor to recognise early need of emergency medical intervention, re-imaging and neurosurgery.   

References and Further Reading

[cite]

From Experts To Our Students! – GIB

Sudden Severe Headache

665-  SAH

In case you didn’t encounter a sudden severe headache today!

A 46-year-old female patient presented with severe headache. BP: 178/88 mmHg, HR: 103 bpm, RR: 22/min, T: 37, SpO2: 98% in room air. She has no history of disease. She is unconscious (GCS E1, V3, M4). No obvious lateralized motor deficit. Bedside gluco-check is normal. You intubated her to secure airway and send her to the CT (above image). What is your next action?

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