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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 wounds.

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Superficial cranial wounds and cranio-cerebral wounds

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  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. 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

  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

  7. 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

  8. 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

  9. 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

  10. Semiology of intracranial surgical diseases

  11. 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

  12. 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

  13. 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

  14. 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

  15. Epidural or extradural hematoma • Develops between dura-mater and endocranium • Clinical signs after accumulation of 15-25 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

  16. 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) 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

  17. 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.

  18. 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

  19. Tumors

  20. 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

  21. 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

  22. 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 Tumors of the skull

  23. 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

  24. 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.

  25. 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

  26. 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

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

  28. 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)

  29. 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

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

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

  32. 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

  33. 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

  34. 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

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

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

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

  38. 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

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

  40. 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

  41. Neck contusions

  42. 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

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

  44. 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-traceal contusion

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