Superficial cranial wounds and cranio-

cerebral wounds

Definition of wounds

A wider concept then usual

Communication with the interior of the cranial cavity can exist with an undamaged skin Venous anastomoses CSF fistula

Wounds Unpenetrated Penetrated Perforant

Unpenetrated woundsOne or more of the strata of the soft tissues and cranial bones without lesions of DURA MATER

Scalp and bony structures

Cerebral lesion can co-exist depending on the nature of the traumatic agent and force of impact

Unpenetrated wounds of the scalp

Cut wounds Sharp weapons or

pieces of glass Sharp edges easy to

suture together Frequently without

underlined lesions

Bloody wounds (rich vascular network)Examination may be difficult and sometimes it is necessary to remove hair from adjacent areas

Unpenetrated wounds of the scalp

Laceration wounds Crushing the scalp

after aggression with a rounded object

Irregular edges as the scalp breaks laterally (difficult to suture together)

Initial bleeding is not major (crushing effect)

Very often associated with bone lesions

Unpenetrated wound of the skull

Fractures of the skull are associated with scalp woundsDifferent type of fractures depending on With lesions involving intracranial structures Neurological topography

Examination: after proper cleaning of the wounds Linear fracture the skull under the wound Depression of protrusion of the skull in a fractured

area Intermediate bone fragments

Unpenetrated wound of the skull

Radiography is essential to evaluate fracture linesCT is better for evaluation of the skull and cerebral lesions. Neurological examination is fundamentalEvery cranial wound is potential penetrated or even perforated

Penetrated wounds Violent impact with injury of all structures overlaying the skull + skull + Dura Mater

It is usually produced in injuries produced through acceleration

Traumatic agent can be impacted in the skull

Unperforated but penetrated wounds are exceptional

One of the major risks is the laceration of the dural venous sinuses with major hemorrhage

Perforant wounds

Violent impact – fractures with intermediate fragmentsDetached bone structures +/- traumatic agent are projected in the cerebrum PROTOTIP: shoot wounds Symptoms Wounds Cerebral lesion: contusion or laceration

Major risk of infection: surgical emergency

Semiology of intracranial surgical diseases

Cerebral concussion

CCT with small energy transfer

Produces a functional lesion of the cerebrum that is completely reversible PATHOLOGICALL IT HAS NO ORGANIC SIGNIFICANCE

Primary it affects the ascending activator system: temporary loss of consciousness, short time +/- vegetative disfunctions

Cerebral contusion

Organic lesion that is mostly reduced to vascular lesions After impact the first phenomenon is paralytic vasodilation with small hemorrhages – can be responsible for an increase in intracranial pressure and compression. In severe forms an intracerebral hematoma is formedThere is a postcontusional syndrome Minor: symptoms are short and completely reversible Moderate: partial reversible and easy to compensate Major: prolonged coma + associated with neurological

phenomena either somatic or visceral type, focal elements for cerebral lesion or brain stem lesion

Cerebral laceration

The typical mechanism is by decelaration

Cerebrum is projected over bonny prominences. Bone fragments my be accelerated in the cerebral mass.

Neurological manifestations depend on the affected site: wide range No symptoms Clinically evident with neurological signs

compatible with a focal lesion

Postraumatic compressive lesions – Intracranial

hematomaBloody collections Well circumscribed Behave like expanding tumors COMPRESSIVE effect over the adjacent cerebrum The fluid collections tend to fill in and develop over the small

reserve spaces (both in quantity and topography)

Produces an increase in the intracranial pressure: major risk for secondary compression of the brain stem through herniation through foramina occipitalae – compression over the respiratory and circulatory nerve centers – MAJOR EMERGENCY – Requires decompression

Epidural or extradural hematoma

Develops between dura-mater and endocranium Clinical signs after accumulation of 15-25 mlMost frequent in the temporal area Dura mater easy to peal-off the temporal bone (Gerard-

Marchand area) Middle meningeal artery and dural venous sinuses

Hematoma increases in size up to a pressure that produces hemostasis (30-100ml of blood)Clinic: coma which appears after a short free interval or minimal posttraumatic symptoms (LUCID INTERVAL)General status and neurological status worsens quickly or progressively: compression of the temporal lobe + controlateral hemiparesisBloody suffusion of the scalp in coresponding area may be suggestive

Subdural hematomaMost common type – bridging vessels from cerebral cortex to major dural sinusesDevelop outside the brain in the subdural spaceClinical signs depend on te speed and existence of extra space (“brain smaller the skull”)Acute(within 24 hours): most frequently produced through lacerations in the fronto-parietal region, associated with major injuries. Bad prognosis even after evacuation (75% death rate) Most – venous, rare arterial and grow faster Compression: focal signs + laterality Pupilary changes in most cases

Subacute (<14 days) chronic (>14 days) Circumscribed by a fibrous capsule Asymptomatic interval = rule (may forget the trauma) Simptoms: headache, papilledema, focal neurological deficit ~ brain

tumor Initially clotted blood that liquefies later and can be extracted by bur

holes

Intracerebral hematoma

Positioned in the cerebral massFollows a contusion or laceration of the brainFocal neurological deficit with or without an asymptomatic lag period. Progressive worsening in a serious cranio-cerebral trauma is highly suggestive.

Intracranian hematomaIn all forms High level of suspicion High death rate associated with negligence Careful follow-up with special attention to “LUCID

PERIOD”Clinical manifestations: neurological focal lesion with left/right asymmetryImagistic : CT, MRI, angiographyNO lumbar punction if intracranial hypertension cannot be ruled out (major risk of herniation)Urgent decompression is compulsory

Tumors

Tumors of the scalp

Sebaceous cysts – embryonic epidermal cell developing in the structure of the skullBenign tumors of the skullFrequently more then oneTend to grow and may become infectedNot painful but estetic problem

Tumors of the skull

LIpoma: Benign tumor developing from fat cells Well circumscribed, soft, lobulated. Easy to

recognize

Vascular tumors: angiomas Congenital hemangiomas: “strawberry-like”

tumors, well circumscribed – may spontaneously regress in month/years

Intradermic diffuse hemangioma (port-wine stain) Spider hemangioma

Tumors of the skull

Benign tumorsOsteomaOsteochondroma

Malignant tumorsOsteosarcomaMultiple mielomaMetastatic

tumors

May be symptom-less and may not be accessible for palpation

Rx: lesion with abnormal bone structure – excessive bone apposition or bone destruction

Final diagnosis - biopsy

Intracranial tumors

Tumoral growth

Pseudo-tumors (any expansive lesion)

SymptomsFocal neurological lesion at onset

(depending on the location of the tumor)Common pathway of evolution: intracranial

hipertension

Focal neuroogical deficit

Depends on the topographical location

Functional significance of the area

EEG and PET can trace a point that triggers functional disorders

Clinical examination : motor and sensorial deficit characteristic to a certain neurological area.

Frontal lob tumors

Unilateral deficit in small tumors: Clinical manifestation mostly psychiatric:

psychic and motor excitement, followed by depression and disorientation

Bilateral (either extension or due to high intracranial pressure) Lack of interest to the outside world.

Reactions triggered only by vegetative needs: FRONTAL LOBOTOMY

Parietal lob tumor

Sensorial epilepsy instead of seizures

Painful or hypoesthesia paroxysms

Changes in sensibility

Abnormalities in the perception of the body of parts of it

Temporal lob tumors

Temporal epilepsy: psycho-motor, psycho-sensorial manifestations, illusions, dream-like status

Olfactive or gustative hallucinations

Paroxistic anxiety or euphoria

Occipital lob tumors

Sensorial changes mostly associated with visual perception: visual hallucinations, homonym hemi-anopsia

Nominal and sensorial aphasia (unable to understand and use of words)

Optic agnosia and alexia (unable to understand written language)

Intracranial hypertension syndrome

Common pathways in the evolution of all expanding processes with intracranial developmentThe increase in intracranial tumor determines: CompressionContra lateral shift of cerebrumDecreased capacity of the skull to host the

brain

Intracranial hypertension syndrome

Causes: Intracranial expanding processes (any)Abnormalities in the flow of the

cerebrospinal fluid (hydrocephalus)Cerebral edema

Clinical signs

HEADACHEAn important sign, not always presentNon-specific It’s significance increases when

Appears in the morningSudden onset

Clinical signs

VOMITINGNot a constant signMore significant when it is manifested in

the morning a jeunFrequently and more significant when it is

not associated with nauseaEarly morning vomiting appears to be

associated with the nocturnal increase in intracranial pressure

Clinical signs

VISUAL CHANGESDOUBLE VISION different palsies of

oculomotor nerves (compression)Papillary edema (fundus examination)

OBJECTIV SIGN – major element in the diagnosis of intracranial hypertension

It does not develop instantly – REQUIRES TIME for edem to be visible

Attention

Signs of intracranial hypertension should be looked for in any patient with questionable expanding intracranial process or cranio-cerebral traumaLumbar puncture (diagnostic reasons) prohibited in cases wit suspicion of intracranial hypertension. MAJOR RISK of sudden death – herniation of the cerebellous amigdala through foramen occipitale and brainstem compression. Urgent decompression

Clinical anatomy and exploration of the neck

Hyoid bone

Thyroid cartilage

Crico-thyroid ligament

Cricoid cartilage

Tracheal rings

Thyroid gland

Suprasternal notchANTERIOR VIEW

Clinical anatomy and exploration of the neck

Occipital protuberance

Processus spinosum of cervical vertebrae + C6 most proeminent one

Paravertebral muscles

Intervertebral ligaments

POSTERIOR

Clinical anatomy and exploration of the neck

Sterno-cleido-mastoidean muscle

Trapesius

Plastima

LATERAL

Anterior triangle of the neck

Istmus of thyroid gland

Vascular sheet Carotid artery Carotid glomus Jugular vein Vagus nerve Lymph nodes of the

juguar vein

Posterior triangle of the neck

Roots and main branches of the brachial plexus

Spinal nerve (XI)

Subclavicular artery

External jugular vein

Parotid gland

Trauma of the neck

Partially exposed to trauma

Vital significance due to the significance of the anatomic elements passing through Many structures – even if individually

injured – can be lethal.Frequently combined injuries

Neck contusions

Soft tissue contusionsLarge muscular groups are primarily affected

SCM in lateral impact and posterior paravertebral muscles in posterior impact Simple contusion Hematomas Muscular ruptures

Laryngo-traceal contusion

Mechanism of traumaAntero-posterior compressionLateral compressionStrangulation

Major traumaDislocation Fracture of thyroid cartilage +/- tracheal

lesions

Laryngo-traceal contusion

Siymptoms Violent pain Major respiratory distress Death via vagus

mediated reflexes or carotid glomus reflexes

Clinical examination

Mild forms Dysphonic or aphonic

(hematoma) Respiratory tract relatively

normal Respiratory distress depending

on the degree of deformation or obstruction (blood or secretions)

Laryngo-tracheal contusion

Major trauma: dislocation or fracture of the laryngo-tracheal conduct Violent pain exacerbated with each

movement Coughing with bloody expectoration Subcutaneous emphysema Abnormal movement of the cartilages Major respiratory distress

Cervical contusions of the vertebrae and spinal cord

MORE OFTEN FRACTURES, seldom dislocationsC1-C2 – major risk Spinal cord compressions due to instability of the

vertebral segment involved in trauma Ischemia: compression over the vertebral arteries Cranio-cerebral trauma may be clinically more

significant TCC and a potentially lethal injury of the cervical vertebrae may be missed

Clinical examination: permanent pain and stiffness due to antalgic contracture

Cervical contusions of the vertebrae and spinal cordDislocations appear via accentuated flexion or extension. Dislocation without neurological signs : limited

disparity minor symptoms Dislocations: dominant neurological presentation

(spinal cord compression) Dislocation of the odontoid process – lethal .

Fractures: compression or direct mechanism Neurological signs depend on relative positions of

vertebrae and spinal cord

ANY CRANIO-CEREBRAL TRAUMA SHOULD BE CONSIDERED AT RISK BEFORE RULLING OUT VERTEBRAL INJURY

FIST AID – IMOBILISATION WTH RIGID COLLAR

Wounds of the neck

Venous wounds

Very dangerous area – veins are adherent to superficial fascia (external jugular vein) or fascia propria (internal jugular vein)

Major risk for gaseous embolus

Massive blood loss in sort time

Arterial wounds

Wounds of the main vessels: massive bleeding – death is possible before medical intervention through exsanguination

Added risk to emergency tracheotomy High tracheotomy : small riskLow tracheotomy: high risk

Complex arterio-venous wounds

Concomitant lesionsDirect consequence: arterio-venous fistulaPulsatile tumorVeins are turgid and pulsate Symptoms generated by compression due

to a growing tumor Compression of the main veinsSympathetic chain: Sdr. Claude-Bernard-

Horner

Laryngo-tracheal wounds

Very much similar with contusions

Always associate important bleeding with acute respiratory distress

Clinical: Characteristic respiratory sound as the air

escapes through the wound Subcutaneous emphysema Difficult coughing with blood in sputum Anxiety and dysphonic

Clinical exploration of the thyroid gland

InspectionPalpationAscultation (seldom)

Inspection

Anterior and midline situated organ of the lower neckUnder the hyoid bone Butterfly shape (2 lobs, one istmus)Attached to trachea via loose connective tissue

Inspection

Palpation

Semiology of inflammatory diseases of the thyroid gland

Thyroiditis

Acute suppurative thyroiditis Young women Usually follows an acute respiratory episode

(produce either by a microbial or viral infection) Sudden onset with thyroid gland enlargement Severe neck pain radiating in the brachial plexus, associated with dysphagia, fever, chills dysphonia and dyspnoea May evolve towards an abscess and needs surgical drainage

Thyroiditis

Subacute thyroiditis (de Quervain)

Granulomatous thyroiditis wit giant cells

Symptoms similar with the acute form but less obvious + clinical signs of thyroid hyperfunction

ThyroiditisChronic thyroiditis

Some specific forms are exceptional (tuberculosis, syphilis) Hashimoto’s thyroiditis Progressive enlargements of the thyroid gland Rubber –like consistence Slow progression with development of fibrosis that

destroys the gland Initially it behaves with hyperfunction and

progresses towards hypofunction in late stages Differential diagnosis with thyroid cancer

Riedel thyroiditis Intense fibrous invasion of the thyroid gland – hard

consistence (wood) Little inflammation – symptoms generated mostly

due to compression

Distrophic lesion of the thyroid gland (goiter)

Endemic goiter

GOITER = any enlargement of the thyroid gland

Hyperplasia of the thyroid tissue and connective tissue and vascular structures due to insufficient iodine intake

May be diffuse or multinodular

Clinical

The thyroid gland is enlarged (normal sizze coresponds to the distal phalanx of the thumb)Uni- or bilobar (typical butterfly shape)Diffuse goiter is the usual formNodular goiter: the NODULE a significant entity If large in volume – may produce compressive effects Intrathoracic goiter

Typical forms according to symptoms

Type I = common form

Type II = hormonal abnormalities

Type III = neurological signs are dominant

Exploration

Morphology of the glandRx cervico-mediastinalScintigraphyCTscan

Hormonal activityNormalHyperthyroidism Hypothyroidism

Clinical signs in hyperthyroidism

Fiziopathology

Excess stimulation of the glandOne nodule becomes autonomus and does not respond to normal feed-back mechanism HIGH ABNORA LEVELS OF THYROIDIAN HORMONES Common symptoms in all form Complex implications

Main conditions

Graves disease

Toxic multinodular goiter (Pierre-Marie)

Toxic adenoma – (Plummer)

Metabolic symptoms

Weight loss – constant and early sign

Changes in thermal homeostasis: hypersensitivity to heat, abundant sweating, warm an moist skin

Symptoms due to sympathetic stimulationCardiovascular symptoms (tachycardia, rhythm abnormalities, late stages cardiac failure)Neurological symptoms – fine tremor of the extremitiesSNS – excessive nervousness, mood swings, emotiveFatigue Digestive symptoms: diarrhea

Genital signs

Less constant

Women: abnomal menstrual bleeding (hypermenorrhea, polymenorrhea), it can be a cause of sterility

Men: decreased sexual drive

Signs away from thyroid gland specific to Graves’

diseaseCan not be reproduced with the administration of thyroid hormones Ophthalmic signs Upper lid retraction – characteristic

view of the face Exophthalmia Upper lid does not elevate during

upwards gaze

Dermatologic signs – pretibial edema (hard non-pitting edema)

Malignant thyroid tumorsESSENTIALS

History of irradiation

Fixed, hard, firm nodule + lymphadenopathy

Normal thyroid function

Malignant thyroid tumors

Clinical characterization:Mostly inadequate,

except for advanced stages

The basis for early diagnosis – evaluation of the thyroid nodule

Thyroid NODULE

Problems:Symptomatic / asymptomaticBenign / malignant

Differentiate between:Benign nodular goiterCystsThyroiditisMalignant tumor

Diagnosis

History (duration, onset, irradiation)Palpation (solitary - more likely malignant)Scintigraphy: cold noduleUltrasound scan – solid tumorHormonal test – non-secretoryAspiration cytology/ core biopsy = essential (pathologic or high suspicion)