Resumen
La terapia eléctrica en cardiología está encaminada a transferir electrones al miocardio, su
mayor utilidad está dada en la cardioversión y desfibrilación. La terapia eléctrica cumple las
leyes de la electricidad y el mayor factor a vencer es la impedancia o resistencia al flujo de
electrones. Para mejorar la efectividad de la terapia eléctrica se han ideado diferentes formas
en la onda de choque, en la duración y la polaridad.
La terapia eléctrica ha logrado consolidarse como el tratamiento de elección del paro cardiorrespiratorio secundario a fibrilación ventricular y taquicardia ventricular sin pulso.
Es igualmente el tratamiento de elección en taquiarritmias con compromiso hemodinámico.
Pese a sus grandes ventajas tiene efectos secundarios que se deben conocer adecuadamente
para dar un tratamiento oportuno.
Palabras clave: electrones, conductividad eléctrica,estimulación eléctrica, energía eléctrica,
electro shock, paro cardíaco, fibrilación ventricular, taquicardia ventricular.

Summary
Electrical shock in cardiology are pursuid transfer of electrons to the myocardium. Its main
indications are`s cardioversion and defibrillation.
The electrical shock therapy follows laws of electricity laws and consequently, its main
difficulty is the impedance or resistance of electrons flow. To make better the effectiveness
of this therapy, a number of improvements have been made on the shock wave, its duration, and
polarity. The electric shock therapy has become the preferred treatment when dealing with
cardiorespiratory arrest secondary, ventricular fibrillation and pulseless ventricular tachycardia.
Similarly, it is the preferred treatment for ventricular tachyarrhythmia associated with
hemodynamic compromise. Despite its significant advantages, this treatment causes
secondary effects, which should adequately be known in order to provide a timely treatment.

Resumen
La terapia eléctrica en cardiología está encaminada a transferir electrones al miocardio, su
mayor utilidad está dada en la cardioversión y desfibrilación. La terapia eléctrica cumple las
leyes de la electricidad y el mayor factor a vencer es la impedancia o resistencia al flujo de
electrones. Para mejorar la efectividad de la terapia eléctrica se han ideado diferentes formas
en la onda de choque, en la duración y la polaridad.
La terapia eléctrica ha logrado consolidarse como el tratamiento de elección del paro cardiorrespiratorio secundario a fibrilación ventricular y taquicardia ventricular sin pulso.
Es igualmente el tratamiento de elección en taquiarritmias con compromiso hemodinámico.
Pese a sus grandes ventajas tiene efectos secundarios que se deben conocer adecuadamente
para dar un tratamiento oportuno.
Palabras clave: electrones, conductividad eléctrica,estimulación eléctrica, energía eléctrica,
electro shock, paro cardíaco, fibrilación ventricular, taquicardia ventricular.

Summary
Electrical shock in cardiology are pursuid transfer of electrons to the myocardium. Its main
indications are`s cardioversion and defibrillation.
The electrical shock therapy follows laws of electricity laws and consequently, its main
difficulty is the impedance or resistance of electrons flow. To make better the effectiveness
of this therapy, a number of improvements have been made on the shock wave, its duration, and
polarity. The electric shock therapy has become the preferred treatment when dealing with
cardiorespiratory arrest secondary, ventricular fibrillation and pulseless ventricular tachycardia.
Similarly, it is the preferred treatment for ventricular tachyarrhythmia associated with
hemodynamic compromise. Despite its significant advantages, this treatment causes
secondary effects, which should adequately be known in order to provide a timely treatment.

Author: Tom Scaletta, MD, Past-President, American Academy of Emergency Medicine; Chairperson, Department of Emergency Medicine, Edward Hospital; Assistant Professor of Emergency Medicine, Rush Medical College and Cook County Hospital

INTRODUCTION

Background

An acute subdural hematoma (SDH) is a rapidly clotting blood collection below the inner layer of the dura but external to the brain and arachnoid membrane. Two further stages, subacute and chronic, may develop with untreated acute SDH. Each type has distinctly different clinical, pathological, and imaging characteristics.

Generally, the subacute phase begins 3-7 days after acute injury. (Surgical literature favors 3 days; radiological literature favors 7).

The chronic phase begins about 2-3 weeks after acute injury.

For a related CME activity, see Medscape's CME - Severe Traumatic Brain Injury: Evolution and Current Surgical Management.

Pathophysiology

Typically, low-pressure venous bleeding of bridging veins (between the cortex and venous sinuses) dissects the arachnoid away from the dura and layers out along the cerebral convexity. Cerebral injury results from direct pressure, increased intracranial pressure (ICP), or associated intraparenchymal insults.

In the subacute phase, the clotted blood liquifies. Occasionally, in the prone patient, the cellular elements layer can appear on CT imaging as a hematocritlike effect.

In the chronic phase, cellular elements have disintegrated, and a collection of serous fluid remains in the subdural space. In rare cases, calcification develops.

Frequency

United States

Frequency is related directly to the incidence of blunt head trauma. An SDH is the most common type of intracranial mass lesion, occurring in about a third of those with severe head injuries (Glasgow Coma Scale [GCS] score less than 9).

Mortality/Morbidity

Acute SDH is associated with high mortality and morbidity rates.

• Simple SDH accounts for about half of all cases and implies that no parenchymal injury is present. Simple SDH is associated with a mortality rate of about 20%.
• Complicated SDH accounts for the remaining cases and implies that parenchymal injury (eg, contusion or laceration of a cerebral hemisphere) is present. Complicated SDH is associated with a mortality rate of about 50%.

Age

The majority of SDHs are associated with age factors related to the risk of blunt head trauma. Certain age factors are related to more unusual variants of this disease.

• SDH is more common in people older than 60 years. The elderly are predisposed to cerebral atrophy because they have less resilient bridging veins. Moreover, these veins can be damaged more easily in the elderly.
• Since the adhesions existing in the subdural space are absent at birth and develop with aging, bilateral SDHs are more common in infants.
• Interhemispheric SDHs are often associated with child abuse.

CLINICAL

History

• Suspect acute subdural hematoma (SDH) whenever the patient has experienced a mechanism of moderately severe to severe blunt head trauma.
• Patients generally lose consciousness, but this is not an absolute.
• Chronic SDH is more difficult to anticipate, and about half of such cases offer no history of head trauma. Patients often present with progressive symptoms such as unexplained headache, personality changes, signs of increased ICP, or hemiparesis/plegia.
• Any degree or type of coagulopathy should heighten suspicion of SDH.
• Hemophiliacs can develop SDH with a seemingly trivial head trauma. An aggressive approach to diagnosis and immediate correction of the factor deficiency to 100% activity is paramount.
• Alcoholics are prone to thrombocytopenia, prolonged bleeding times, and blunt head trauma.

• Maintain a high level of suspicion in this population.
• Promptly obtain a CT scan of the head when the degree of trauma is severe, focal neurologic signs are noted, or intoxication does not resolve as anticipated.
• In alcoholics, more than any other cohort, acute or chronic SDHs can be due to the deadly combination of repetitive trauma and alcohol-associated coagulopathies.

Patients on anticoagulants can develop SDH with minimal trauma and warrant a lowered threshold for obtaining a head CT scan.

Physical

• Physical examination of patients with head trauma should emphasize assessment of neurologic status using the GCS. Search for any focal neurologic deficits or signs of increased ICP.
• Signs of external trauma alert the physician to the expected location of coup or contrecoup injuries on CT scan.
• Any abnormality of mental status that cannot be explained completely by alcohol intoxication or the presence of another mind-altering substance should increase suspicion of SDH in the patient with blunt head trauma. Obtain an urgent CT scan.
• GCS score less than 15 after blunt head trauma, in a patient with no intoxicating substance use (or impaired mental status baseline), warrants consideration of an urgent CT scan.
• Presence of a focal neurologic sign following blunt head trauma is ominous and requires an emergent explanation.

WORKUP

Lab Studies

• Complete blood count
• Coagulation profile
• Electrolytes
• Type and screen/cross

Imaging Studies

• While MRI is superior for demonstrating the size of an acute subdural hematoma (SDH) and its effect on the brain, noncontrast head CT is the primary means of making a diagnosis and suffice for immediate management purposes.
• Acute SDH typically appears on a noncontrast head CT scan as a hyperdense (white) crescentic mass along the inner table of the skull, most commonly over the cerebral convexity in the parietal region (see Media file 1). The second most common area is above the tentorium cerebelli.

• Small SDHs may blend in with the adjacent skull and may be appreciated only by adjusting the CT window width to between those generally used to view brain and bone.
• Some degree of midline shift should be present with moderate or large SDHs. Suspect a contralateral mass when midline shift is absent. If midline shift seems excessive, suspect underlying cerebral edema.
• SDHs are relatively uncommon in the posterior fossa since the cerebellum undergoes little movement, which is protective of its bridging cortical veins. SDHs that do occur in that location are usually a result of parenchymal cerebellar injury.
• Interhemispheric SDH causes the falx cerebri to appear thickened and irregular and often is associated with child abuse.

• In the subacute phase, the lesion becomes isodense (with respect to the brain) and is more difficult to appreciate on a noncontrast head CT scan (see Media file 2).

• For this reason, either contrast-enhanced CT or MRI is widely recommended for imaging 48-72 hours after head injury.
• On T1-weighted MR images, subacute lesions are hyperdense.
• On contrast-enhanced CT scans, cortical veins over the cerebral surface are opacified and help delineate the lesion.
• Subacute SDHs often become lens-shaped and can be confused with an epidural hematoma.

• In the chronic phase, the lesion becomes hypodense and is easy to appreciate on a noncontrast head CT scan.
• A worsening of the GCS by 2 or more points should prompt repeat imaging in salvageable patients.

TREATMENT

Emergency Department Care

• Consider endotracheal intubation when GCS score is less than 12 or other indications are present; this guarantees airway protection during the diagnostic workup.
• Obtain an immediate head CT scan in patients with head trauma who experienced clear loss of consciousness, are symptomatic, are disoriented/amnestic, or have any focal neurologic signs.
• Elevate the head of the bed to 30 degrees and make sure that the head and neck are maintained in a midline position to optimize venous outflow from the brain.
• Hyperventilation to a target pCO₂ of 30 mm Hg can reduce ICP in the short term though pCO₂
• Burr holes are a temporizing option when rapid demise is associated with severe head trauma, especially if a herniation syndrome is clinically evident.
• Burr holes can guide surgical therapy when head CT imaging is unavailable.
• Begin on the side of the (first) dilated pupil.
• Generally, because the lesion represents clotted blood, the burr hole is not curative, and emergent craniotomy is necessary.

less than 25 mm Hg is strongly discouraged.

Consultations

When a patient who experienced head trauma presents with a GCS score less than 12, consider immediate neurosurgical consultation while stabilizing and diagnostic maneuvers are in progress.

• Small, asymptomatic, acute SDHs may be managed by observation, serial examinations, and serial CT scanning.
• Patients with focal findings, neurologic worsening, hematoma greater than 1 cm thick, midline displacement/shift greater than 5 mm, or increased intracranial or posterior fossa pressure require operative intervention.
• The usual treatment for acute SDH is craniotomy and evacuation by a neurosurgeon.
• After making a large cranial flap, open the dura.
• Remove the clot with suction, cup forceps, and/or irrigation. Identify and control bleeding sites.

MEDICATION

• Glucocorticoids are not indicated for head trauma.
• Intravenous mannitol (0.25 g/kg) may be used to decrease ICP.

FOLLOW-UP

Transfer

• Detected subdural hematomas (SDHs) require patient transfer to facilities offering neurosurgical evaluation and treatment.
• Transfer may be emergent, with appropriate stabilization measures taken and with appropriately skilled personnel accompanying the patient.

Complications

• Postoperative complications
• Elevated ICP
• Brain edema
• New or recurrent bleeding/hematoma
• Infection
• Seizures
• Chronic SDH
• Recurrent hematoma (50%)
• Infection (eg, subdural empyema, wound)
• Seizures (up to 10%)

Prognosis

• Definitive prognosis often is not possible at the time of emergency department evaluation.
• Advanced age, presenting GCS less than 8, extension of blood into the intraventricular space, and uncontrolled ICP are factors associated with significantly reduced survivability.
• Ultimate prognosis is related to the amount of associated direct brain damage and the damage resulting from the mass effect of the SDH.

MISCELLANEOUS

Medical/Legal Pitfalls

• Failure to identify a patient with SDH and delayed diagnosis of the hematoma are constant risks.
• Consider neuroimaging for patients taking anticoagulants.
• Alcoholics may have an associated coagulopathy placing them at high risk for SDH. Altered mental status may be from an SDH, not ethanol.
• Consult a neurosurgeon as soon as the diagnosis is suspected and initiate transfer if a another facility is required for diagnosis or management.

Media file 1: Acute subdural hematoma. Note the bright (white) image properties of the blood on this noncontrast cranial CT scan. Note also the midline shift. Image courtesy of J. Stephen Huff, MD.
	View Full Size Image
Media type: CT

Media file 2: Subacute subdural hematoma. The crescent-shaped clot is less white than on CT scan of acute subdural hematoma (see Media file 1). In spite of the large clot volume, this patient was awake and ambulatory. Image courtesy of J. Stephen Huff, MD.
	View Full Size Image
Media type: CT

REFERENCES

• Bell RS, Neal CJ, Lettieri CJ, Armonda RA. Severe Traumatic Brain Injury: Evolution and Curent Surgical Management. Medscape. Available at http://www.medscape.com/viewprogram/14717_pnt. Accessed June 24, 2008.
• Bullock MR, Chesnut R, Ghajar J, Gordon D, Hartl R, Newell DW. Surgical management of acute subdural hematomas. Neurosurgery. Mar 2006;58(3 Suppl):S16-24; discussion Si-iv. [Medline].
• Buntain BL. Craniocerebral injuries. In: Management of Pediatric Trauma. WB Saunders; 1995:177-88.
• Eijkenboom M, Gerlach I, Barker A, et al. Chronic cognitive effects of bilateral subdural haematomas in the rat. Neuroscience. 2004;124(3):523-33. [Medline].
• Gean AD. Imaging of Head Trauma. Raven Press; 1994.
• Rockswold GL, Tintinalli JE, ed. Emergency Medicine: A Comprehensive Study Guide. 4^th ed. McGraw-Hill; 1996:1142.
• Saito T, Kushi H, Makino K, Hayashi N. The risk factors for the occurrence of acute brain swelling in acute subdural hematoma. Acta Neurochir Suppl. 2003;86:351-4. [Medline].
• Valadka AB, Narayan RK. Injury to the cranium. In: Trauma. 3^rd ed. 1996:267-78.