SURGERY April 2020

CLOSED HEAD INJURY Natakneng 2020

Revalida Reviewer Mariano Marcos State University

Outline MEDICAL MANAGEMENT

Introduction  Patients with a documented CHI and evidence of intracranial hemorrhage or a
Initial Assessment depressed skull fracture should receive a 17-mg/kg phenytoin loading dose,
Medical Management followed by 1 week of therapeutic maintenance phenytoin, typically 300 to 400
mg/d.
Classification
 Phenytoin prophylaxis has been shown to decrease the incidence of early
Types posttraumatic seizures. There is no evidence to support long-term use of
Concussion prophylactic antiepileptic agents.
Contusion  Blood glucose levels should be closely monitored by free blood sugar checks
DIA and controlled with sliding scale insulin.
Traumatic Intracranial Hematoma  Fevers also should be evaluated and controlled with antipyretics, as well as
Epidural Hematoma source-directed therapy when possible.
Acute Subdural Hematoma  Hyperglycemia and hyperthermia are toxic to injured neurons and contribute to
Chronic Subdural Hematoma secondary injury.
Intraparenchymal Hemorrhage  Head-injured patients have an increased prevalence of peptic ulceration and GI
bleeding.
 Peptic ulcers occurring in patients with head injury or high ICP are referred to
as Cushing’s ulcers. Ulcer prophylaxis should be used.
 There are two important factors that affect the outcome of CHI in general.
 Compression stockings or athrombic pumps should be used when the patient
 The initial impact causes the PRIMARY INJURY, defined as the immediate
cannot be mobilized rapidly for prophylaxis of deep venous thrombosis.
injury to neurons from transmission of the force of impact.
 Subsequent neuronal damage due to the sequelae of trauma is referred to as
CLASSIFICATION
SECONDARY INJURY.
 TBI can be classified as mild, moderate, or severe.
 Hypoxia, hypotension, hydrocephalus, intracranial hypertension, thrombosis,
and intracranial hemorrhage may all be mechanisms of secondary injury.  For patients with a history of head trauma, classification is as follows:
GCS
INITIAL ASSESSMENT 3-8 MILD
 The first three elements of the ABCDs of resuscitation— airway, breathing, 9-12 MODERATE
and circulation—must be assessed and stabilized. 13-15 SEVERE
 Hypoxia and hypotension are known to worsen outcome in TBI (due to
secondary injury), making cardiopulmonary stabilization critical.  TBI patients who are asymptomatic, who have only headache, dizziness, or
 Patients who cannot follow commands require intubation for airway protection scalp lacerations, and who did not lose consciousness, have a low risk for
and ventilator control. intracranial injury and may be discharged home without a head CT scan.
 The fourth element, assessment of “D,” for disability, is undertaken next.  Patients with a history of altered consciousness, amnesia, progressive
headache, skull or facial fracture, vomiting, or seizure have a moderate risk for
 Motor activity, speech, and eye opening can be assessed in a few seconds
intracranial injury and should undergo a prompt head CT.
and a GCS score assigned.
 If the CT is normal, and the neurologic examination has returned to baseline
(excluding amnesia of the event), then the patient can be discharged to the care
of a responsible adult, again with printed criteria for returning to the emergency
room. Otherwise the patient must be admitted for a 24-hour observation period.
 Patients with depressed consciousness, focal neurologic deficits, penetrating
injury, depressed skull fracture, or changing neurologic examination have a high
risk for intracranial injury. These patients should undergo immediate head
CT and admission for observation or intervention as needed.

The following is an example of how a primary surveyor may efficiently assess
disability and GCS:
 Approach the patient and enter his or her field of view. Observe whether the
patient is visually attentive. Clearly command: “Tell me your name.”
 Then ask the patient to lift up two fingers on each side sequentially, and
wiggle the toes.
 A visually or verbally unresponsive patient should be assessed for response
to peripheral stimuli such as nail-bed pressure, or deep central painful
stimulation, such as a firm, twisting pinch of the sensitive supraclavicular
skin.
 Watch for eye opening and movement of the extremities, whether
purposeful or reflexive.
 Assess the verbal response. The motor, verbal, and eye-opening scores
may be correctly assigned using this rapid examination.
 An initial assessment of the probability of significant head injury can be
made, assuming that pharmacologic and toxic elements have not obscured
the examination.
 The surveyor must also take note of any external signs of head injury,
including bleeding from the scalp, nose, or ear, or deformation of the skull
or face.
TYPES OF CHI
CONCUSSION
 defined as temporary neuronal dysfunction following non-penetrating head
trauma.
 The head CT is normal, and deficits resolve over minutes to hours.
 Definitions vary;
 some require transient loss of consciousness, while others include
patients with any alteration of mental status
 Memory difficulties, especially amnesia of the event, are very common
 Studies have shown that the brain remains in a hypermetabolic state for up to
a week after injury.
 The brain is also much more susceptible to injury from even minor head trauma
in the first 1 to 2 weeks after concussion (second-impact syndrome)
CONTUSION
 bruise of the brain, and occurs when the force from trauma is sufficient to cause
breakdown of small vessels and extravasation of blood into the brain
 The contused areas appear bright on CT scan
 The frontal, occipital, and temporal poles are most often involved.
 Contusions themselves rarely cause significant mass effect as they represent
small amounts of blood in injured parenchyma rather than coherent blood clots.

Nani Schwartz, Sabiston 1 of 3

SURG 32: CLOSED HEAD INJURY

 Edema may develop around a  Prognosis after successful evacuation is better for EDH than subdural
contusion, causing mass effect. Contusions hematoma (SDH).
may enlarge or progress to frank hematoma,
particularly during the first 24 hours.
 Contusions also may occur in brain
tissue opposite the site of impact (contre-
coup injury). These contusions result from
deceleration of the brain against the skull.

DIFFUSE AXONAL INJURY

 caused by damage to axons throughout the brain, due to rotational acceleration
and then deceleration.
 Axons may be completely disrupted and then retract, forming axon balls.
 Small hemorrhages can be seen in more severe cases, especially on MRI.
 Hemorrhage is classically seen in the corpus callosum and the dorsolateral
midbrain.
EPIDURAL HEMATOMA
 EDH is the accumulation of blood between the skull and the dura.
 EDH usually results from arterial disruption, especially of the middle meningeal
artery.
 The dura is adherent to bone, and some pressure is required to dissect between
the two.
EDH has a classic, three-stage clinical presentation that is probably seen in only
20% of cases.
 The patient is initially unconscious from the concussive aspect of the head
trauma.
 The patient then awakens and has a “lucid interval,” while the hematoma
subclinically expands.
 As the volume of the hematoma grows, the decompensated region of the
pressure-volume curve is reached, ICP increases, and the patient rapidly
becomes lethargic and herniates.
 Uncal herniation from an EDH classically causes ipsilateral third nerve palsy
and contralateral hemiparesis.
ACUTE SUBDURAL HEMATOMA
 result of an accumulation of blood between the arachnoid membrane and
the dura.
 Acute SDH usually results from venous bleeding, typically from tearing of a
bridging vein running from the cerebral cortex to the dural sinuses.
 Elderly and alcoholic patients are at higher risk for acute SDH formation after
head trauma due to brain atrophy.
 On head CT scan, the clot is bright or mixed-
density, crescent- shaped (lunate), may have a
less distinct border, and does not cross the midline
due to the presence of the falx.
 Most SDHs occur over the cerebral hemispheres,
but they may also occur between the hemispheres
or layer over the tentorium.
 Open craniotomy for evacuation of acute SDH is
indicated for any of the following:
 thickness >1 cm,
 midline shift >5 mm,
 or GCS drop by two or more points from the time of injury to
hospitalization.
 Nonoperatively managed hematomas may stabilize and eventually reabsorb, or
evolve into chronic SDHs.
 The prognosis for functional recovery is significantly worse for acute SDH than
EDH because it is associated with greater primary injury to brain parenchyma
from high-energy impacts.

 On head CT the blood clot is bright, biconvex

in shape (lentiform), and has a well-defined
border that usually respects cranial suture
lines.
 An EDH is typically found over the convexities
but may rarely occur in the posterior fossa as
well.
 Open craniectomy for evacuation of the
congealed clot and hemostasis generally is indicated for EDH.
 Patients who meet all of the following criteria may be managed conservatively:
 clot volume <30 cm3,
 maximum thickness <1.5 cm, and
 GCS score >8

NANI Schwartz, Sabiston 2 of 3

SURG 32: CLOSED HEAD INJURY

CHRONIC SUBDURAL HEMATOMA

 Chronic SDH is a collection of blood breakdown products that is at least 2 to 3
weeks old.
 Acute hematomas are bright white (hyperdense) on CT scan for approximately
3 days, after which they fade to isodensity with brain, and then to hypodensity
after 2 to 3 weeks.
 A true chronic SDH will be nearly as dark as CSF on CT.
 Traces of white are often seen due to small, recurrent hemorrhages into the
collection. These small bleeds may expand the collection enough to make it
symptomatic (acute-on-chronic SDH)
 Chronic SDHs often occur in patients without a clear history of head trauma, as
they may arise from minor head injury.
 Alcoholics, the elderly, and patients on anticoagulation are at higher risk for
developing chronic SDH.
 Patients may present with headache, seizure, confusion, contralateral
hemiparesis, or coma.
 A chronic SDH >1 cm or any symptomatic SDH should be surgically drained.
 Unlike acute SDH, which consists of a thick, congealed clot, chronic SDH
typically consists of a viscous fluid with the texture and dark brown color
reminiscent of motor oil.
 A simple burr hole can effectively drain most chronic SDHs.
 The procedure is converted to open craniotomy if the SDH is too congealed for
irrigation drainage, the complex of membranes prevents effective drainage, or
persistent hemorrhage occurs that cannot be reached with bipolar cautery
through the burr hole.
 follow-up head CT scans are required postoperatively and approximately 1
month later to document resolution.

INTRAPARENCHYMAL HEMORRHAGE
 most often associated with hypertensive hemorrhage or arteriovenous
malformations (AVMs).
 Typically occurs in basal ganglia and internal capsule (Charcot-Bouchard of
lenticulostriate vessels)
 Bleeding may occur in a contused area of brain.
 Mass effect from developing hematomas may present as a delayed neurologic
deficit.
 Delayed traumatic intracerebral hemorrhage is most likely to occur within the
first 24 hours.
 Patients with contusion on the initial head CT scan should be reimaged 24 hours
after the trauma to document stable pathology.
 Indications for craniotomy include:
 any clot volume >50 cm3 or
 a clot volume >20 cm3 with referable neurologic deterioration (GCS 6–
8) and associated midline shift >5 mm or basal cistern compression

NANI Schwartz, Sabiston 3 of 3