Sunday, March 21, 2021

Subdural Hematoma Case File

Posted By: Medical Group - 3/21/2021 Post Author : Medical Group Post Date : Sunday, March 21, 2021 Post Time : 3/21/2021
Subdural Hematoma Case File
Lydia Conlay, MD, PhD, MBA, Julia Pollock, MD, Mary Ann Vann, MD, Sheela Pai, MD, Eugene C. Toy, MD

Case 29
A 76-year-old woman suffers a fall at home. She appears uninjured, but the next day becomes progressively forgetful, drowsy, and disoriented, so she is taken to the emergency room (ER) for evaluation. According to her family, the patient’s only medical problem is chronic atrial fibrillation, for which she takes warfarin. Her review of symptoms is otherwise reportedly normal. 

On physical examination, the patient’s blood pressure is 180/110 mm Hg, HR 90 bpm, and respirations 12 breaths per minute. She opens her eyes to painful stimuli, but will neither communicate nor cooperate with a neurological examination. A CT scan of the head reveals an acute subdural hematoma (SDH), with a midline shift of 6 mm. Laboratory studies show a hematocrit of 32 and an INR of 4.3. Her ECG shows diffuse, deep, symmetrical T-wave inversions. An urgent neurosurgical consult is obtained and the patient is emergently taken to the OR for a craniotomy to evacuate the hematoma.

➤ What is the most important priority for an anesthesiologist in a patient with an acute subdural hematoma who has rapidly-deteriorating neurological signs?

➤ How should the above patient be evaluated preoperatively?

➤ What are the anesthetic goals for patients presenting for an evacuation of a subdural hematoma?

Subdural Hematoma

Summary: This elderly, anticoagulated patient presents with an acute subdural hematoma following a fall.
Most important priority: To promptly provide conditions suitable for an evacuation of the hematoma. This consideration supersedes almost all others.

Preoperative evaluation: In the acute setting, there is little time to conduct a formal pre-anesthetic assessment. Moreover, the patient may not be capable of responding to questions. Knowledge of any allergies to medications, pre-existing medical conditions (which may need to be obtained from the patient’s family), the circumstances of his or her injury, and a quick airway assessment may well be all that time allows.

Anesthetic goals: In addition to the goals for any type of anesthetic (to maintain stability of the vital functions, provide an insensitivity to pain, prevent awareness, and optimize the surgical field), the anesthetic goals for evacuation of a subdural hematoma are to maintain adequate cerebral perfusion pressure, and to prevent or attenuate increases in ICP and cerebral edema throughout the perioperative period.


1. Understand the etiology of subdural hemorrhage, and the characteristics of the patients most at risk.
2. Become familiar with the Glasgow coma scale and its impact on the decision for surgery.
3. Understand the concept of autoregulation, how it can be altered, and the consequences of doing so.
4. Become acquainted with the challenges of emergence following a neurosurgical procedure, and its associated risks.

Since this patient requires emergent evacuation of the SDH, as described earlier, the preoperative assessment is abbreviated to the few questions that are absolutely necessary, and these are often asked and answered as an intravenous catheter and monitors are placed.

A quick assessment of her “ABCs” allows the rapid formulation of an appropriate anesthetic plan. “Airway” examines the potential for difficult airway management or intubation. “Breathing” assesses her ventilatory status





Eye opening


To verbal command

To pain






Best verbal response

Oriented, conversing

Disoriented, conversing

Inappropriate words

Incomprehensible sounds

No verbal response






Best motor response

Obeys verbal commands

Localizes to pain


Abnormal flexion decorticate

Extension (decerebrate)

No response (flaccid)







and oxygenation, and “circulation” examines her hemodynamic stability. The patient’s neurological status is also categorized using the Glasgow coma scale (please see Table 29–1).

This patient requires general anesthesia with an endotracheal tube, a large bore intravenous access for aggressive fluid resuscitation, and the availability of blood products. Fresh frozen plasma and vitamin K are indicated to reverse the coagulopathy as soon as possible.

No premedication is indicated given the patient’s depressed level of consciousness. Monitoring includes standard monitors (5-lead ECG, pulse oximetry, capnography, noninvasive blood pressure monitoring), urine output, body temperature, and train-of-four.

An intra-arterial blood pressure catheter is ideal, but given the acuity of the patient’s neurological status, a prompt induction to allow rapid evacuation of the hematoma may take precedence. Induction is accomplished with propofol, thiopental, or etomidate. Etomidate is preferable, since significant
hypotension may follow administration of the former two. In this patient with severe arterial hypertension likely reflecting a high ICP, any significant reduction in arterial pressure would rapidly reduce cerebral perfusion and thus lead to cerebral ischemia.

Paralysis is achieved with a nondepolarizing muscle relaxant, and the anesthetic is maintained with an opioid and an inhalation agent as tolerated. Postoperatively, she will most likely be kept intubated and will receive positive pressure ventilation in an intensive care unit.

Subdural Hematoma

SUBDURAL HEMATOMA (SDH): An accumulation of blood in the subdural space between the dural and arachnoid layers of the meninges. This condition primarily occurs over the surface of a cerebral hemisphere, but may develop in the posterior fossa and spinal canal. SDH may be acute or chronic.
ACUTE SUBDURAL HEMATOMA (ACUTE SDH): Is usually caused by tearing of the bridging veins that drain from the surface of the brain to the dural sinuses. Rupture of these vessels allows for bleeding into the space between the arachnoid membranes and dura. Venous bleeding is usually arrested by the rising intracranial pressure or direct compression by the clot itself. Trauma to the cortical arteries accounts for approximately 20% to 30% of SDH cases.
GLASGOW COMA SCALE: Quantifies neurological impairment in the setting of head injury in terms of eye opening, speech, and motor function. The maximum score that can be obtained is 15, and severe head injury is determined by a score of 8 or less persisting for 6 hours or more. The numerical points assigned to patients in the Glasgow coma scale are illustrated in Table 29–1. An indication for ICP monitoring is an acute SDH with GCS score less than 9.
CEREBRAL PERFUSION PRESSURE (CPP): Is the net pressure gradient causing blood flow to the brain (brain perfusion). CPP is calculated as the difference between mean arterial pressure (MAP) and intracranial pressure (ICP).

Cerebral Perfusion Pressure (CPP) = MAP × ICP or CVP
(whichever is higher)

CEREBRAL AUTOREGULATION: Is a protective mechanism that maintains cerebral blood flow between mean arterial pressures (MAP) of 50 and 150 mm Hg by adjusting cerebral vascular resistance. Hypertensive patients demonstrate a shift of autoregulation to a higher blood pressure. Thus, their lower level of autoregulation could be well above 50 mm Hg, and their upper limit of autoregulation similarly increased.

Autoregulation can be abolished by trauma, hypoxia, and certain anesthetics. When blood pressure falls below the autoregulated range, cerebral ischemia can occur. When blood pressure exceeds the autoregulated range, cerebral blood flow increases markedly, thus rapidly increasing ICP, potentially disrupting the blood-brain barrier, and even causing cerebral edema. Similarly, severe intracranial hypertension can actually precipitate reflex arterial hypertension and bradycardia (Cushing triad). A rapid reduction in systemic blood pressure in these patients may precipitate cerebral ischemia by reducing cerebral perfusion pressure.

A SDH is considered acute if the patient becomes symptomatic within 72 hours of an insult or injury, subacute between 3 and 15 days, and chronic after 2 weeks. The neurological findings associated with an acute SDH may include an altered level of consciousness, a dilated or nonreactive pupil ipsilateral to the hematoma, and/or hemiparesis contralateral to the hematoma. An acute SDH typically requires a craniotomy for evacuation of the clot and decompression of the brain, while burr holes can be used to achieve the same for chronic SDH. Both subacute and chronic SDHs are usually observed in patients over 50 years of age.

Head trauma is the most common cause of SDH, with the majority of cases resulting from motor vehicle accidents, falls, and assaults. Patients with significant cerebral atrophy are particularly at risk. This category includes the elderly, those with a history of chronic alcohol abuse, and those with previous traumatic brain injury. In such patients, trivial head trauma or even whiplash injury in the absence of physical impact may produce a SDH. Similarly, the use of antithrombotic agents also increases the risk of SDH. In one series, treatment with oral anticoagulants, aspirin, or heparin at the time of hemorrhage was present in 21%, 13%, and 5% of patients with chronic SDH following head trauma.

The estimated mortality rate for patients requiring surgery for SDH is 40% to 60%. In patients who present with coma, the mortality rate approaches the higher end of that range. Age and neurological status as assessed with the Glasgow coma scale are also important prognostic indicators for patients with SDH.

The indications for surgical evacuation of SDH are:

1. SDH thickness > 10 mm, or midline shift > 5 mm on CT regardless of the GCS score
2. When SDH thickness < 10 mm or midline shift < 5 mm
a. If the GCS starts at < 9 and deteriorates by 2 points or more
b. Pupils are asymmetric or fixed and dilated
c. ICP > 20 mm of Hg

Anesthetic Management of Emergent Craniotomy for Acute SDH
The principal goals of the anesthetic management for a patient with SDH are the preservation of adequate cerebral perfusion pressure and oxygen delivery, the avoidance of secondary brain damage, and the provision of optimal operating conditions.

One of the major concerns is the maintenance or reduction of ICP, particularly in the preoperative period and during induction. The volume inside the cranium is fixed, so if any of the components located in the cranial vault increase in volume, others must decrease or the ICP will increase. When the cranium is open, ICP equals atmospheric pressure, and cerebral perfusion pressure thus equals MAP. Cerebral perfusion pressure should be maintained at a minimum or 60 and 100 mm Hg systolic to prevent secondary ischemic damage.






Volatile anesthetics








No effect/


No effect/




No effect/





IV anesthetics




















No effect/


No effect/



No effect/

No effect/

The specific effects of individual drugs on cerebral vasomotor tone and cerebral metabolic rate are summarized in Table 29–2. Ensuring an adequate depth of anesthesia, controlling blood pressure to avoid hypertensive crises, maintaining cerebral perfusion, and striving for a physiological ICP are more important than the choice of any particular anesthetic drug.

The changes in CBF caused by anesthetic drugs reflect the drug’s individual effects on cerebral vasomotor tone and metabolic rate. In the normal brain, a reduction in cerebral metabolic rate causes cerebral vasoconstriction and reduces CBF, counteracting the vasodilatory effect of the drug. Cerebral vasomotor tone and metabolic rate can be affected to a different extent at different concentrations. Consequently, despite the direct cerebral vasodilatory effects of volatile anesthetics, CBF remains relatively unchanged at concentrations of up to 1 MAC.

However, in patients with an acute brain injury and particularly in the presence of an increased ICP, it is advisable to avoid all anesthetic drugs that dilate cerebral vessels (ie, volatile anesthetics). Instead, agents causing vasoconstriction are preferred (ie, intravenous anesthetics except ketamine).

In the presence of an elevated ICP, thiopental is most commonly used to induce anesthesia, if the patient can tolerate the hypotension that may result. Alternative agents such as propofol or etomidate are also acceptable. In addition, lidocaine is often administered intravenously 90 seconds prior to intubation to suppress laryngeal reflexes, and esmolol may be used to reduce heart rate and blood pressure in response to laryngoscopy.

For paralysis, the possible benefits of a short-acting muscle relaxant (succinylcholine) must be weighed against the risks. Succinylcholine can transiently and modestly increase ICP, an effect which is attenuated by pretreatment with a nondepolarizer. However nondepolarizing muscle relaxants are often preferred instead.

A popular maintenance regimen for neurosurgical patients is a continuous infusion of propofol with remifentanil or fentanyl. In a hemodynamically stable patient with severe intracranial hypertension, narcotics in conjunction with a thiopental infusion (2-3 mg/kg/h) and a nondepolarizing muscle relaxant are sometimes administered with oxygen and air. However, the sedative effects of barbiturates or benzodiazepines can cause postoperative sedation, and thus impede a patient’s ability to cooperate with a neurological examination. In patients with less severe intracranial hypertension, anesthesia is typically maintained with various combinations of barbiturates, narcotics, and sub-MAC concentrations of a volatile anesthetic.

Cerebral Blood Flow and PaCO2
Increasing arterial carbon dioxide levels cause vasodilation and an increase in cerebral blood flow. As a good rule of thumb, increasing the carbon dioxide tension from 40 to 80 mm Hg doubles cerebral blood flow; reducing the carbon dioxide from 40 to 20 mm Hg halves it. These changes are transient, and cerebral blood flow returns to normal within 6 to 8 hours even if the altered carbon dioxide levels are maintained. After induction of anesthesia, in the presence of a subarachnoid hemorrhage (SAH) care must be taken to maintain a normal PaCO2. If a reduction in ICP is desired, only transient and moderate hyperventilation should be considered.

Fluid Management
The two most important principles of fluid management in the neurosurgical patient are to avoid any reductions in serum osmolality to prevent cerebral edema (ie, “keep ‘em dry”), but to remember to treat the “whole” patient, and not just the patient’s brain. Traumatic head injuries may be associated with other types of traumatic injuries, particularly injuries of the chest, and may be signaled by an ongoing fluid requirement.

The patient should be normovolemic, and serum osmolality normal or slightly elevated to minimize cerebral edema. Hypovolemia is associated with cerebral ischemia and perioperative neurological deficits, especially in patients with cerebral vasospasm. Dextrose containing solutions should be avoided because glucose administration increased the incidence of neurologic deficits in experimental models. Infusing large volumes of hypo-osmolar crystalloid solutions such as lactated Ringer solution may predispose to brain edema and contribute to hyponatremia. Therefore, the use of normal saline is preferable.

Central venous pressure (CVP) catheter placement can help to guide intravascular volume status, but is not the priority. Cannulation of the internal jugular vein requires the Trendelenburg position and turning of the head, both of which can critically increase ICP. A large catheter in the internal jugular vein can also impede venous drainage from the head. Patients presenting with an acute SAH are frequently coagulopathic, another relative contraindication to central venous cannulation. Most importantly, the priority is to evacuate the hematoma, and this consideration supersedes almost all others.

Serum sodium is maintained within normal limits, to help maintain serum oncotic pressure and to avoid the hyponatremia associated with cerebral salt wasting and the syndrome of inappropriate secretion of the antidiuretic hormone (SIADH). Hypertonic saline solutions can be useful for volume resuscitation because they lower ICP, increase blood pressure, and produce an osmotic diuretic effect on the brain similar to that of other hyperosmolar solutions, such as, mannitol. However, studies have shown that marked hypernatremia can result from the combination of hypertonic saline and mannitol.

Blood loss during surgery requires transfusion of cross-matched or fresh whole blood. A minimum hematocrit between 30% and 33% is recommended to maximize oxygen transport.

Brain “Relaxation” and Bulk
When the dura is opened, the brain readily demonstrates the suitability of operating conditions. On one hand, it may be bulging, almost pulsating, and appear “tense,” as though it is under pressure (of course, as previously mentioned, the intracranial pressure at that time equals atmospheric pressure). On the other hand, the brain may appear “relaxed,” generally indicating an absence of the signs associated with the “full” or “tense” brain.

If the brain appears “tense,” the methods for reducing brain volume include hyperventilation to decrease cerebral blood flow, diuresis (usually mannitol, Lasix or hypertonic saline), the drainage of cerebrospinal fluid (by ventriculostomy or more frequently a lumbar drain), and reducing MAP (if autonomic dysregulation is present), and less frequently, suppression of the cerebral metabolic rate which also reduces cerebral blood flow (usually with barbiturates).

Emergence from Anesthesia and Surgery
Extubation is a perilous time for patients who have just undergone neurosurgery. Studies have shown the relationship between perioperative hypertension and the development of postoperative hematomas. Yet patients must also be sufficiently awake and oriented so that a neurological examination can be performed. The trick is to provide a rapid and smooth transition from the anesthetized state to being fully awake.

One significant challenge is the patient’s response to the large foreign body in his trachea, namely the endotracheal tube. “Bucking” or coughing on the endotracheal tube can cause arterial hypertension and elevated ICP. Precautions to avoid coughing, straining, hypercarbia, and large swings in blood pressure include lidocaine administered before extubation, beta blockers to control blood pressure, and other antihypertensives if needed during emergence. The patient’s head should be elevated by 15 to 30 degrees, but with consideration to the fact that this position increases the likelihood of aspiration.

Monitoring and Management of Intracranial Hypertension
Following the removal of an intracranial hematoma, the control of ICP is of paramount importance in the patient’s recovery. It is common practice to monitor ICP in the postoperative period in these patients, since those with ICPs below 20 to 25 mm Hg tend to have significantly better outcomes than patients with elevated ICP. Various techniques are used to measure ICP including ventricular catheters, subdural and subarachnoid bolts, epidural transducers, and intraparenchymal fiberoptic devices. Table 29–3 outlines the commonly used measures to control intracranial hypertension.

Systemic Sequelae of Head Injury
In addition to the potentially devastating effects on brain tissue, the systemic effects of head injury are diverse. Many (maybe even most) patients manifest ECG changes in their ST segments and T waves following traumatic brain injury. Head injury can also result in autonomic dysfunction, even life-threatening arrhythmias. Pulmonary problems can include airway obstruction, hypoxemia, adult respiratory distress syndrome, and neurogenic pulmonary edema. Gastrointestinal problems including stress ulcers are common, and may lead to hemorrhage. Pituitary dysfunction as evidenced by diabetes insipidus, SIADH, salt wasting, and metabolic problems such as ketotic hyperosmolar syndrome and/or hyperglycemic coma, and abnormalities of temperature regulation may also occur.

But one of the most important points to remember when caring for patients with head injury is that whatever injured the head may have also injured other parts of the body.






Mannitol (0.25-1g/kg i.v.).

Furosemide (0.5-1mg/kg i.v. alone or 0.15-0.3 mg/kg i.v. in combination with mannitol).




Effective for localized cerebral edema; requires 12-36 hours for full effect

Adequate ventilation

PaO2 ≥100 mm Hg, PaCO2 33-35 mm Hg; hyperventilation on demand.

Optimize hemodynamics

Target normotension and maintain CPP to avoid cerebral ischemia.

Fluid therapy

Target normovolemia before anesthetic induction to

prevent hypotension.Use glucose free iso-osmolar

crystalloid solutions to prevent increase in brain water

content (from hypo-osmolality) and ischemic brain damage

(from hyperglycemia).


To improve venous return (neutral, head-up position).

Reduce CMRO2

Using pharmacologic agents, eg, thiopental and propofol.

Temperature control

Avoid hyperthermia preoperatively, consider mild

intraoperative hypothermia.

CSF drains

To acutely reduce brain tension.

Comprehension Questions

29.1. Which of the following is the most important indication for the surgical evacuation of a SDH?
A. A GCS score of 3
B. A recent history of fall accompanied by a change in mental status
C. Headache
D. GCS score of 10 that deteriorates to 6

29.2. Which of the following therapeutic maneuvers reduce ICP?
A. Hypotonic saline
B. An ICP drain
C. Isoflurane
D. Succinylcholine

29.3. In which of the following locations is an ICP monitor contraindicated?
A. Lumbar spinal drain
B. Subdural catheter
C. Ventriculostomy catheter
D. Intra-parenchymal catheter
E. Epidural catheter

29.1. D. A deterioration of the GCS score or in pupillary signs are indications for surgery. A low GCS alone is not an indication for surgical evacuation of SDH. It is important to quantify any midline shift and thickness of the SDH by CT, and to measure ICP in order to triage this patient. A midline shift of 6 mm, a SDH thickness of 15 mm, a GCS score of 10 that deteriorates to 6, and an ICP of 25 mm of Hg are criteria for the evacuation of an SDH. A recent history of fall accompanied by a change in mental status may be suggestive of intracranial pathology, but in and of itself, does not indicate surgery.

29.2. B. Furosemide, an ICP drain, mannitol, and hypertonic saline are interventions which reduce ICP. Answer C, volatile anesthetics, may decrease CMRO2, but they also cause a dissociation between CMROand CBF. Thus, their direct vasodilatory effect predominates and causes an increase in cerebral blood volume and ICP. Succinylcholine either has no effect on ICP, or reduces ICP in patients with altered intracranial compliance. 

29.3. A. Lumbar drains are contraindicated for the same reason that spinal anesthesia is contraindicated in patients with elevated ICP: the danger of transforaminal herniation. All the other locations can be used for monitoring ICP.

Clinical Pearls
➤ The anesthetic goals for the evacuation of a subdural hematoma are to maintain adequate cerebral perfusion pressure,and to prevent or attenuate increases in ICP and cerebral edema throughout the perioperative period.
➤ While invasive arterial monitoring is desirable for anesthesia for a craniotomy, a rapidly deteriorating neurological status may take precedence.
➤ Traumatic head injuries may be associated with other types of traumatic injuries, particularly injuries of the chest.
➤ Severe intracranial hypertension can precipitate reflex arterial hypertension and bradycardia (Cushing triad). A rapid reduction in systemic blood pressure in these patients may precipitate cerebral ischemia by reducing cerebral perfusion pressure.


Barash PG, Cullen BF. Clinical Anesthesia. 5th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2005. 

Bullock MR, Chesnut R, Ghajar J, et al. Surgical management of acute subdural hematomas. Neurosurgery. 2006;58 (3 suppl):S16-S24; discussion si-iv. 

Bullock R, Chesnut RM, Clifton G, et al. Guidelines for the management of severe head injury. Brain Trauma Foundation. Eur Emerg Med. 1996;3(2):109-127. 

Cenic A, Bhandari M, Reddy K. Management of chronic subdural hematoma: A national survey and literature review. Can J Neurol Sci. 2005;32(4):501-506. 

Ernestus RI, Beldzinski P, Lanfermann H, Klug N. Chronic subdural hematoma: Surgical treatment and outcome in 104 patients. Surg Neurol. 1997;48(3):220-225. 

Gennarelli TA, Spielman GM, Langfitt TW, et al. Influence of the type of intracranial lesion on outcome from severe head injury. J Neurosurg. 1982;56:26. 

Kotwica Z, Brzezinski J. Acute subdural haematoma in adults: An analysis of outcome in comatose patients. Acta Neurochir (Wien). 1993;121:95. 

Miller RD. Miller’s Anesthesia. 6th ed. Philadelphia, PA: Elsevier Churchill Livingstone; 2005. 2-volume set. 

Reymond MA, Marbet G, Radu EW, Gratzl O. Aspirin as a risk factor for hemorrhage in patients with head injuries. Neurosurg Rev. 1992;15:21. 

Samudrala S, Cooper PR. Traumatic intracranial hematomas in neurosurgery. Neurosurgery. 1996;2797-2807. 

Stanisic M, Lund-Johansen M, Mahesparan R. Treatment of chronic subdural hematoma by burr-hole craniostomy in adults: influence of some factors on postoperative recurrence. Acta Neurochir (Wien). 2005 Dec;147(12):1249-56. 

Weigel R, Krauss JK, Schmiedek P. Concepts of neurosurgical management of chronic subdural haematoma: Historical perspectives. Br J Neurosurg. 2004;18(1): 8-18.


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