The curious case of Kevin, A cat and SDH

Lisa Housel NARJake Sareerak NAR

Samuel Merritt UniversityAnatomy and Physiology

65 yo Male presenting to physician with c/o HA x 1 week Hit head on porch while searching for his cat

Headache began at this time or shortly after HA continue to occur after arguments with wife

Symptoms: Continuous HA, all over head and extend to posterior neck

muscles Tight neck muscles Vision and hearing are WNL Denies nausea Hasn’t been sleeping well No relief with APAP and ibuprofen

Case Study

A&Ox3 VS are WNL Neck is supple and FROM Tympanic membrane, optic reflexes and retinae

are intact Steady gait and DTR intact Diagnosed with muscle tension headache and

treated with sedative, muscle relaxant and pain medication Call MD if HA does not improve over the weekend

Physical Examination

Returns to physician on Monday morning due to no improvement

in HA Appearance and manners are changed from Friday Unable to drive Drowsy Increased pain; throbbing when supine or flexes neck Vision intact Diminished appetite; denies emesis BP=140/90 (Friday=120/80) FROM in neck; flexion increases HA Cranial nerve, optic, and gait/balance tests are WNL and

symmetrical Skull=tender to touch

Follow-up

Blood tests (CBC, WBC, Differential) WNL CT scan of the head reveals a large, bilateral

subdural hematoma of uncertain age Absence of skull fx

Diagnostic Tests

Referred to neurosurgeon

Performs craniotomy with evacuation of hematoma

Per surgeon, when skull pierced, blood is initially released at a high pressure

HA minimal after surgery; good spirits with family at bedside

Treatment

Primary Traumatic Brain Injury:Result of immediate mechanical disruption of brain tissue.

Shear injury

Contusion

Intraparenchymal hematoma

Subarachnoid hemorrhage

Subdural hematoma

Epidural hematoma

Skull fracture

Diffuse brain swelling

Vascular injuries

Cervical spine injury

Airway Management:

Intubation: Indications for TBI patients:– Respiratory distress.– Motor posturing/absence of response to pain.– Hypoxia/hypercapnia.– GCS < 8.– Seizures.– Increased ICP.– Need for analgesics/sedatives.– Significant associated injuries.

Secondary Brain Injury:Pathophysiological response to primary neuronal injury

Hours to days after primary insult.

Progressive.

Hypoxia/hypotension are main causes for 2nd injury.

High ICP.

Hyperthermia.

Brain edema.

Hemorrhage .

The primary focus of neurocritical care for TBI is the prevention, identification, and treatment of

secondary brain injury.

Subdural Hematoma Tearing of bridging veins:

• Secondary to acceleration/deceleration.• Cresent shaped hematoma.• Hematoma much slower to develop

(venous origin) into a mass large enough to produce sx

Damage due to impact:• Higher impact than that of EDH. • More brain injury and edema.

Treatment:• Symptomatic > 1 cm thick at its biggest point• Smaller subdurals may be observed.

Mortality:• Range is 50-90%.

High mortality rate if:• Delay of surgery is > 4 hrs.• Patient is on anticoagulants.• Poor neurological grade on admission.

Type Occurrence

after InjuryProgression of Symptoms

Treatment

Acute 24-48 Hr after severe trauma

Immediate deterioration

Craniotomy, evacuation and decompression

Subactue 48 hr-2 wk after sever trauma

Initial unconsiousness, gradual improvement, deterioration over hours, dilation of pupils, ptosis

Evacuation and decompression

Chronic Weeks, months, usually > 20 days after injury; often injury seemed trivial or forgotted by patient

Nonspecific, nonlocalizing progression; progressive alteration in LOC

Evacuation and decompression, membranectomy

Types of SDH

Classification of Head (Brain) Injury

Minimal no loss of consciousness

or amnesia GCS 15

Mild amnesia or brief (< 5 min)

LOC, or impaired alertness, memory

GCS 14-15 Post-concussive syndrome

Moderate LOC > 5 min, or focal

neurologic deficit GCS 9-13

Severe GCS < 8

Glasgow Coma ScaleBest Motor Response:

Obeys 6Localizes pain 5Flexion withdrawal 4Flexion abnormal (decorticate)

3Extension (decerebrate) 2No response 1

Best Verbal Response:Oriented and converses 5Disoriented and converses

4Inappropriate words 3Incomprehensible sounds 2No response 1

Eye Opening:Spontaneously 4To verbal stimuli 3To pain 2Never 1

3-15

The peak incidence of SDH is in the 6th and 7th

decades of life when a larger SD space is available as a result of brain atrophy

The enlarged space accounts for the presenting complaint of focal symptoms rather than those associated with increased ICP

Symptoms may mimic other health problems: somnolence, confusion, lethargy, and memory loss.

SDH in Elderly

Headache results from blood accumulation

between the dura mater and arachnoid layer causing an increase in ICP

Headache also results from brain compression; SDH slowly enlarges due to repeated bleeding until a mass effect occurs

Headache is usually severe or moderately severe, and in the first few days after the injury, the headache is apt to be constant.

It’s usually generalized, however sometimes it could be localized to the aspect of the hematoma.

Possible Causes of Headache

Current headache is continuous

Common symptom due to the mass effect of hematoma causing increase ICP and cerebral edema

Headache is all over his head, and extends into his posterior neck muscles, which are tight SDH was bilateral in origin, therefore, no lateralization occurred Stiffness of the neck and neck pain could additionally be

present when blood has been extravasated into the sub-arachnoid space

Vision and hearing are normal and he has no nausea Visual and hearing deficits would be noted with an ICH SDH is located between the dura and arachnoid space which

causes pressure; venous in nature and usually slow bleed. Would have nausea if pressure (ICP) was higher, therefore, his

SDH was diagnosed in time to prevent secondary injury

Significance of Symptoms

APAP and Ibuprofen did not relieve headache WHY???

HA related to blood in subdural space increasing ICP Skull is rigid, inelastic container that houses the brain, blood

volume and CSF Since inelastic container, only small increases in volume within

the compartment can be tolerated before pressure increases dramatically (concept is defined by Monro-Kellie Doctrine)

Intracranial volume is fixed; if pressure in compartment rises, compensatory action occurs but is limited

APAP and Ibuprofen are NSAIDs that inhibit COX1 and COX2 which leads to the inhibition of prostaglandin synthesis and decreased formation of precursors Analgesia is probably produced via peripheral action in which

blockade of pain impulse generation results from decreased prostaglandin activity.

Tylenol and Ibuprofen

What is the significance of each of the following findings: Kevin was alert & oriented, and his vital signs were normal; his neck was supple and had normal range of motion; his skull was normal on palpation; there were no signs of abnormal cranial nerve function; his tympanic membranes were normal, as were his optic reflexes and retinae; his gait and deep tendon reflexes were also normal? What possible problems were ruled out in the course of this examination?

His symptoms did not correlate with neurological deficits that would result from a dramatic increase in ICP or herniation

His symptom reflect the ability for the intracranial compartment to compensate for the extra blood by decreasing CSF production to attempt to maintain homeostasis in relation to pressure

SDH was no longer growing in size or the bleed was slow in progression, therefore, symptoms were not dramatic as seen in a SAH.

Results of Physical Exam

Inability to drive Drowsy Worsening of headache Increased throbbing pain when lying down Lack of appetite

Significance of symptoms?

Blood collected in the subdural space draws

water due to osmosis Further compressing brain tissue Causing new bleeds by tearing other blood

vessels

Pathophysiology

So much room within the skull Rigid box 80% occupied by brain tissues 10% Blood supply 10% by CSF

ICP

Why?????? HOB 15 to 45 degree < ICP HOB > 45 degree < CPP HOB flat > ICP = More headache and pain Positioning--HOB elevated with head midline

to avoid impeding venous return

Increased throbbing pain when lying down?

Depends on the size of the hematoma and the

degree of any associated parenchymal brain injury

headache, nausea, confusion, personality change, decreased level of consciousness, speech difficulties, other change in mental status, impaired vision or double vision, and weakness

A dilated or nonreactive pupil ipsilateral to the hematoma (or earlier: a pupil with a more limited range of reaction)

Hemiparesis contralateral to the hematoma.

Clinical Presentations

Cranial Nerve Optic Gait/balance Asymmetry = involvement at the center of the

brain Signs and symptoms depend on the severity

and location

Symmetry vs Asymmetry?

Bilateral fixed and dilated pupils are secondary to inadequate cerebral perfusion Cerebral hypoxia and severe increased ICP

Pupils that are fixed and dilated Irreversible injury

A unilateral fixed (unresponsive) and dilated pupil Involvement of optic nerve

A unilateral dilated pupil that does not respond to either direct or consensual stimulation transtentorial herniation

A core optic pupil is a pupil that appears irregular in shape midbrain injuries

A finding of significant asymmetry during the

motor examination may be indicative of a hemispheric injury and raises the possibility of a mass lesion. Midbrain controls ocular motion Pons coordination of eye and facial movement Hearing and balance

Balance and Gait

Signs of Cerebral Herniation

Unconscious/unresponsive Patient

Asymmetric pupils.

Dilated or fixed pupil(s): unilaterally or bilaterally.

Unresponsive to painful stimuli.

Patient displays posturing.

First abnormal flexion: decorticate.

Then abnormal extension: deceberate.

Cushing’s Triad may be present:

Bradycardia, apnea and hypertension.

Significance of normal vs abnormal blood test

Abnormal CBC, Electrolytes….. PT/PTT and Plts: defective coagulation H/H may be low WBC normal to slightly elevated Toxicology panel for altered patient to r/o

substances abused Abnormal laboratory values may need to be

corrected…ie. Increased INR due to coumadin and Plts dysfunction

Blood test

What does this indicates?

High ICP

High Opening Pressure