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Superficial cranial wounds and cranio- cerebral wounds.

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Presentation on theme: "Superficial cranial wounds and cranio- cerebral wounds."— Presentation transcript:

1 Superficial cranial wounds and cranio- cerebral wounds

2 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

3 Unpenetrated wounds One 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

4 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

5 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

6 Unpenetrated wound of the skull Fractures of the skull are associated with scalp wounds Different 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

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8 Unpenetrated wound of the skull Radiography is essential to evaluate fracture lines CT is better for evaluation of the skull and cerebral lesions. Neurological examination is fundamental Every cranial wound is potential penetrated or even perforated

9 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

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11 Perforant wounds Violent impact – fractures with intermediate fragments Detached 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

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13 Semiology of intracranial surgical diseases

14 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

15 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 formed There 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

16 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

17 Postraumatic compressive lesions – Intracranial hematoma Bloody 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

18 Epidural or extradural hematoma Develops between dura-mater and endocranium Clinical signs after accumulation of ml Most 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 hemiparesis Bloody suffusion of the scalp in coresponding area may be suggestive

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20 Subdural hematoma Most common type – bridging vessels from cerebral cortex to major dural sinuses Develop outside the brain in the subdural space Clinical 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) 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

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22 Intracerebral hematoma Positioned in the cerebral mass Follows a contusion or laceration of the brain Focal neurological deficit with or without an asymptomatic lag period. Progressive worsening in a serious cranio-cerebral trauma is highly suggestive.

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24 Intracranian hematoma In 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 asymmetry Imagistic : CT, MRI, angiography NO lumbar punction if intracranial hypertension cannot be ruled out (major risk of herniation) Urgent decompression is compulsory

25 Tumors

26 Tumors of the scalp Sebaceous cysts – embryonic epidermal cell developing in the structure of the skull Benign tumors of the skull Frequently more then one Tend to grow and may become infected Not painful but estetic problem

27 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

28 Tumors of the skull Benign tumors Osteoma Osteochondroma Malignant tumors Osteosarcoma Multiple mieloma Metastatic 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

29 Intracranial tumors Tumoral growth Pseudo-tumors (any expansive lesion) Symptoms Focal neurological lesion at onset (depending on the location of the tumor) Common pathway of evolution: intracranial hipertension

30 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.

31 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

32 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

33 Temporal lob tumors Temporal epilepsy: psycho-motor, psycho-sensorial manifestations, illusions, dream-like status Olfactive or gustative hallucinations Paroxistic anxiety or euphoria

34 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)

35 Intracranial hypertension syndrome Common pathways in the evolution of all expanding processes with intracranial development The increase in intracranial tumor determines: Compression Contra lateral shift of cerebrum Decreased capacity of the skull to host the brain

36 Intracranial hypertension syndrome Causes: Intracranial expanding processes (any) Abnormalities in the flow of the cerebrospinal fluid (hydrocephalus) Cerebral edema

37 Clinical signs HEADACHE An important sign, not always present Non-specific It’s significance increases when Appears in the morning Sudden onset

38 Clinical signs VOMITING Not a constant sign More significant when it is manifested in the morning a jeun Frequently and more significant when it is not associated with nausea Early morning vomiting appears to be associated with the nocturnal increase in intracranial pressure

39 Clinical signs VISUAL CHANGES DOUBLE 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

40 Attention Signs of intracranial hypertension should be looked for in any patient with questionable expanding intracranial process or cranio- cerebral trauma Lumbar 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

41 Clinical anatomy and exploration of the neck Hyoid bone Thyroid cartilage Crico-thyroid ligament Cricoid cartilage Tracheal rings Thyroid gland Suprasternal notch ANTERIOR VIEW

42 Clinical anatomy and exploration of the neck Occipital protuberance Processus spinosum of cervical vertebrae + C6 most proeminent one Paravertebral muscles Intervertebral ligaments POSTERIOR

43 Clinical anatomy and exploration of the neck Sterno-cleido-mastoidean muscle Trapesius Plastima LATERAL

44 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

45 Posterior triangle of the neck Roots and main branches of the brachial plexus Spinal nerve (XI) Subclavicular artery External jugular vein Parotid gland

46 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

47 Neck contusions

48 Soft tissue contusions Large muscular groups are primarily affected SCM in lateral impact and posterior paravertebral muscles in posterior impact Simple contusion Hematomas Muscular ruptures

49 Laryngo-traceal contusion Mechanism of trauma Antero-posterior compression Lateral compression Strangulation Major trauma Dislocation Fracture of thyroid cartilage +/- tracheal lesions

50 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)

51 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

52 Cervical contusions of the vertebrae and spinal cord MORE OFTEN FRACTURES, seldom dislocations C1-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

53 Cervical contusions of the vertebrae and spinal cord Dislocations 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

54 ANY CRANIO-CEREBRAL TRAUMA SHOULD BE CONSIDERED AT RISK BEFORE RULLING OUT VERTEBRAL INJURY FIST AID – IMOBILISATION WTH RIGID COLLAR

55 Wounds of the neck

56 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

57 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 risk Low tracheotomy: high risk

58 Complex arterio-venous wounds Concomitant lesions Direct consequence: arterio-venous fistula Pulsatile tumor Veins are turgid and pulsate Symptoms generated by compression due to a growing tumor Compression of the main veins Sympathetic chain: Sdr. Claude-Bernard- Horner

59 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

60 Clinical exploration of the thyroid gland

61 Inspection Palpation Ascultation (seldom)

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

63 Inspection

64 Palpation

65 Semiology of inflammatory diseases of the thyroid gland

66 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

67 Thyroiditis Subacute thyroiditis (de Quervain) Granulomatous thyroiditis wit giant cells Symptoms similar with the acute form but less obvious + clinical signs of thyroid hyperfunction

68 Thyroiditis Chronic 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

69 Distrophic lesion of the thyroid gland (goiter)

70 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

71 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 form Nodular goiter: the NODULE a significant entity If large in volume – may produce compressive effects Intrathoracic goiter

72 Typical forms according to symptoms Type I = common form Type II = hormonal abnormalities Type III = neurological signs are dominant

73 Exploration Morphology of the gland Rx cervico-mediastinal Scintigraphy CTscan Hormonal activity Normal Hyperthyroidism Hypothyroidism

74 Clinical signs in hyperthyroidism

75 Fiziopathology Excess stimulation of the gland One 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

76 Main conditions Graves disease Toxic multinodular goiter (Pierre-Marie) Toxic adenoma – (Plummer)

77 Metabolic symptoms Weight loss – constant and early sign Changes in thermal homeostasis: hypersensitivity to heat, abundant sweating, warm an moist skin

78 Symptoms due to sympathetic stimulation Cardiovascular symptoms (tachycardia, rhythm abnormalities, late stages cardiac failure) Neurological symptoms – fine tremor of the extremities SNS – excessive nervousness, mood swings, emotive Fatigue Digestive symptoms: diarrhea

79 Genital signs Less constant Women: abnomal menstrual bleeding (hypermenorrhea, polymenorrhea), it can be a cause of sterility Men: decreased sexual drive

80 Signs away from thyroid gland specific to Graves’ disease Can 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)

81 Malignant thyroid tumors ESSENTIALS History of irradiation Fixed, hard, firm nodule + lymphadenopathy Normal thyroid function

82 Malignant thyroid tumors Clinical characterization: Mostly inadequate, except for advanced stages The basis for early diagnosis – evaluation of the thyroid nodule

83 Thyroid NODULE Problems: Symptomatic / asymptomatic Benign / malignant Differentiate between: Benign nodular goiter Cysts Thyroiditis Malignant tumor

84 Diagnosis History (duration, onset, irradiation) Palpation (solitary - more likely malignant) Scintigraphy: cold nodule Ultrasound scan – solid tumor Hormonal test – non-secretory Aspiration cytology/ core biopsy = essential (pathologic or high suspicion)


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