Superficial cranial wounds and cranio- cerebral wounds.
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Transcript of Superficial cranial wounds and cranio- cerebral wounds.
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)